Greetings, and welcome to the INmune Bio second 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 touch-tone phone. 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 Mr. Daniel Carlson, Head of Investor Relations at INmune Bio. Daniel? Thank you, operator, and good afternoon, everyone. We thank you for joining us for the call for INmune Bio's second quarter 2025 financial results. Presenting on today's call are David Moss, Co-Founder and CEO; Dr. C.J. Barnum, Head of Neuroscience; and Dr. Mark Lowdell, Chief Scientific Officer and Co-Founder of INmune Bio. Before we begin, however, I remind everyone that except for statements of historical fact, 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 is 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. Now it's my pleasure to turn the call over to our CEO, David. Good afternoon, everyone, and thank you for joining us for this investor update. I'm David Moss, and I'm honored to address you today as the new Chief Executive Officer of INmune Bio. I've had the pleasure to meet many of our shareholders over the years, and as many of you know, I'm very excited with the opportunity with INmune Bio's three therapeutic platforms and the opportunity they present to patients and shareholders. Before we dive into our progress, I want to take a moment to acknowledge R.J. Tesi, who has retired and resigned as President and CEO, Chief Medical Officer, Chairman of the Board, and co-founder of INmune Bio. Along with Mark, myself, and the team at INmune Bio, we acknowledge that R.J. has been a driving force behind INmune Bio, and his leadership has positioned us for the opportunities we're discussing today. As R.J. transitions to retirement, we wish him all the best and extend our deepest gratitude for his contributions. I'm excited to step into this role and build on the strong foundation he has laid. Let's start with XPro and the results from our phase II MINDFuL trial. The trial was designed to define the patient population for a registration trial, and I'm pleased to report that the data confirms that patients with Alzheimer's disease who exhibit two or more biomarkers of inflammation are the optimal candidates for XPro. The trial confirms our original hypothesis and fully aligns with our novel approach to Alzheimer's that XPro would benefit patients with the most inflammation, especially in a short trial. As C.J. will speak about in more detail shortly, I want to emphasize something that I think is really important about phase II studies, which is that the purpose of a phase II trial is to inform the design of a phase III program, of which clear identification of the target population is critical. These findings reinforce our hypothesis that XPro is uniquely suited to address Alzheimer's disease patients with elevated inflammation levels, a group we estimate that comprises somewhere between 40% - 60% of all Alzheimer's cases. We believe strongly that we have a potential first-in-class drug to treat Alzheimer's that is unique and differentiated from current treatments. We believe the XPro program represents a significant opportunity for a strategic partner. Advancing to the next phase will require substantial investment in manufacturing and clinical trials, but we believe the potential is massive. Big Pharma routinely takes on programs at this stage, and we believe XPro could be transformative in addition, and a transformative addition to their pipelines addressing a critical unmet need in Alzheimer's disease. While we have not yet entered into any strategic partnerships, we have begun exploring potential opportunities and have held preliminary conversations with a limited number of parties. XPro is a unique drug that has potential multi-targeted therapeutic applications that could be very meaningful to the right partner and our shareholders, and we intend to prudently pursue these avenues while also being creative to advance them on our own with limited resources. Beyond Alzheimer's, XPro has a multi-targeted drug with broad potential. We are actively exploring the shorter, faster pathways to market, including opportunities potentially in rare disease to maximize its impact and accelerate patient access. Targeting the rare disease pathway would enable us to bring XPro to market faster with more efficient use of resources. We'll provide updates on these efforts in the future. Our immediate next steps for XPro and AD include publishing the trial results in a peer-reviewed journal and preparing a briefing book for our end-of-phase II meeting with the FDA, which we expect to occur before year's end. While AD trials are inherently challenging, the data from this study underscores XPro's potential as a best-in-class treatment for Alzheimer's patients with inflammation. This is a significant development for patients, families, and our shareholders, and we're committed to charting the best path forward with XPro. Before I move to CORDStrom, I want to highlight that the company has made the decision to not pursue treatment-resistant depression at this time. We are reevaluating the best opportunity for XPro beyond AD that combines efficiencies with cost and the shortest timeline to approval for targeted diseases where TNF plays a vital role. These likely include rare diseases, as I mentioned earlier. Now turning to CORDStrom, we believe there is tremendous underappreciated value to this program, and our focus is clear: securing approval in the UK and US for recessive dystrophic epidermolysis bullosa, or RDEB. We anticipate filing for approval in both jurisdictions by mid-year 2026. Importantly for us, we believe that Congress is likely to pass the Give the Kids a Chance Act that would extend the PRV and a priority review voucher program through 2029. We believe that CORDStrom will qualify for a PRV if approved in the U.S. Critically or clinically, we believe CORDStrom has shown tremendous promise, and its potential extends beyond RDEB to other forms of EB. We also see additional opportunities for CORDStrom to expand to other indications. Depending on available capital, we'll aim to develop these opportunities internally with non-dilutive funding or partnerships to ensure we fully realize CORDStrom's value. Finally, I'd like to touch on INKmune. Our phase I/II program is near completion, and as Mark will detail shortly, the data demonstrate that INKmune is safe and delivers immunologic benefits. Like many immunotherapies, think checkpoint inhibitors, Herceptin, et cetera, INKmune is most effective when administered earlier in the disease course, targeting residual disease rather than late-stage metastatic disease with heavy tumor burden. Immunotherapies require time and multiple doses to achieve their full effect. With this in mind, we plan to explore a trial focused on earlier-stage disease to optimize INKmune's potential. Before I turn this call over to the rest of the team, I'd like to thank all of our investors for our continued support. It's an honor to take over the role of CEO, and I'm confident in our path forward and excited about the opportunities ahead. We have a tremendous team of people and exciting clinical programs, and the opportunities in front of us, I'll now hand, and to describe the opportunities in front of us, I'll now hand it over to C.J. to dive deeper into the XPro data. C.J. Thank you, David, and good afternoon, everyone. I am pleased to share the latest updates on our XPro program, a novel approach that continues to show promise as a potential treatment for Alzheimer's disease. Our phase II clinical trial has marked an important milestone in XPro's development, providing both encouraging data and valuable insights. While the trial did not meet its primary endpoint in the overall population, it revealed notable benefits in a key subgroup: Alzheimer's patients with a high burden of inflammation. These patients are identified by the presence of at least two inflammatory biomarkers at baseline. In this subgroup, we observed an effect size of 0.27 on the primary endpoint EMAC and 0.23 on a key secondary behavioral endpoint, the neuropsychiatric inventory. Although modest, these effect sizes are comparable to or even exceed those achieved by currently approved Alzheimer's disease therapies, indicating that XPro could provide a meaningful real-world benefit for patients with high inflammation. Furthermore, favorable trends were noted across multiple endpoints, with effect sizes nearing 0.2 in other cognitive measures, patient-reported outcomes, and biomarker data. Notably, biomarker trends, including pTau217 and GFAP, suggest that XPro is effectively targeting underlying neurodegenerative processes in alignment with its anti-inflammatory mechanism. These findings underscore the potential of XPro as a promising therapeutic option for Alzheimer's patients. For potential partners, the key question is whether there's a clear signal and a viable path to phase III. We believe the answer is a resounding yes. Early feedback from the Alzheimer's Association International Conference indicates strong interest from industry partners who recognize the promising results as appropriate for this stage of development and emphasize the clear, actionable path forward. The feedback we received highlights that partners see XPro as a unique and compelling opportunity in Alzheimer's treatment, extended beyond cognitive benefits to address critical areas of behavior and safety. Its targeted effectiveness in patients with high inflammation reinforces the hypothesis that XPro delivers the greatest impact within this subgroup, providing meaningful benefits to those who need it most. Furthermore, improvements in the neuropsychiatric inventory scores demonstrate its ability to reduce behavioral symptoms, issues that often weigh more heavily on caregivers than cognitive decline. This positions XPro as a comprehensive solution for Alzheimer's care. Perhaps most importantly, the complete absence of amyloid-related imaging abnormalities, or ARIA events, even in high-risk patients underscores its exceptional safety profile, distinguishing XPro as a safer and potentially complementary option for combination therapies. With its unique blend of targeted efficacy, behavioral benefits, and unmatched safety, XPro stands out as an innovative and broadly appealing option in Alzheimer's treatment. We're excited to further explore these opportunities. Some investors have raised questions about why we missed the primary endpoint in the overall population. The explanation is straightforward: the placebo group did not decline. It is impossible to test a drug's ability to slow, stop, or reverse disease progression if the comparison group remains stable. We initially expected that one inflammatory biomarker would be sufficient to show decline over six months. This was not the case. In this cohort, a higher inflammatory burden was necessary. This is part of the learning process. Additionally, our data revealed that six months is not enough time to observe potential functional benefits of XPro in this cohort. While this is unfortunate, it's not entirely unexpected, as functional improvement often lags behind cognitive improvements and can require longer trials to demonstrate meaningful differences. This, too, is part of the learning process and underscores why clinical development progresses through multiple phases. Each phase builds on the previous one, providing the critical information needed to advance. Our phase II trial, MINDFuL, has successfully achieved that objective. Looking ahead, we're preparing to apply for breakthrough therapy designation with the FDA, which could expedite XPro's path forward. We are also planning an end-of-phase II meeting with the FDA to align on the design of our phase III trial. Additionally, we are actively exploring strategic partnerships to support the program's continued advancement. These steps are essential to maintaining our momentum and bringing XPro to patients as quickly as possible. We are deeply encouraged by these results and remain steadfast in our commitment to advancing XPro as a novel, safe, and effective therapy for Alzheimer's disease. I look forward to sharing further updates as we progress towards phase III and work to make a meaningful difference for patients and their families. Now I'll hand the call over to Mark to discuss our other platforms. Thanks, C.J., and good afternoon, everyone. Thanks for joining the call. As David said, CORDStrom has shown great promise in the randomized control trial in RDEB, but its potential extends way beyond RDEB to other forms of epidermolysis bullosa and indeed other conditions and indications, as David alluded. First, we have to remember that the orphan drug designation we received last year was awarded for all forms of epidermolysis bullosa, not just RDEB, and the excellent safety data and ease of administration in the real-world clinical setting that we saw in the RDEB trial mean that we're well placed to treat a much wider group of adult and indeed pediatric EB sufferers, and we're developing plans for this. However, the umbilical cord-derived MSC product we've developed is truly revolutionary in the MSC field since it's manufactured from four individual umbilical cord MSC products. It gives it excellent stability, unlike conventional MSC drugs, and crucially allows us to tailor the final product to target different disease indications. Because we can test the potency of the individual single cord MSC seed stocks for different functional characteristics, we can then combine a specific number of four with the optimal potencies for different indications to create a different type of CORDStrom. For example, the CORDStrom product for RDEB can be made from four MSC seed stocks with the best wound healing capacity and those which secrete the right cytokines to enhance wound repair and suppress itch. For an indication such as osteoarthritis, however, we would select MSC seed stocks with the greatest secretion of anti-inflammatory factors. At the moment, we're investigating many other potential indications, and we'll consider genetic modification of CORDStrom products to deliver specific proteins, such as the collagen seven protein in gene, which is missing in patients with RDEB. Depending on available capital, we aim to develop these opportunities internally or through strategic partnerships to ensure we fully realize CORDStrom's value. As a company, we're keenly focused on preparing the market authorization application for the U.K. and the biologics license application for the U.S. by mid-2026, as David said. Now, we understand the aggressiveness of these timelines, and I'll not bore you with all of the details required to meet these goals, but I would like to thank our team in the U.K. for working so hard to keep these timelines and remain confident that the external third parties who we have to work with and who are critical to this will also remain on track to allow us to meet this timeline. On the other side, with regards to INKmune, we've continued to develop the manufacturing data to support commercial development and make it the least expensive cellular drug in the field of oncology. In Q1 this year, we closed the phase I aspect of our phase I/2 care PC trial in metastatic prostate cancer, having met the primary safety endpoint. Importantly, this didn't only confirm safety of INKmune at three dose levels, but it also demonstrated the ease with which it could be delivered to patients in a day clinic setting without hospitalization overnight. This is unique in the field of a cellular oncology drug. We moved into the phase II trial stage of the trial in February and started to receive the blinded patient blood monitoring samples from the phase I patients. It became apparent very rapidly that some patients were responding to INKmune as predicted, with an increased number of NK cells in their circulation and in vivo stimulation of memory-like function. Independent analysis of the PSMA PET scans, which is the assay we've chosen to measure disease burden, showed that despite worsening disease in all of these heavily pretreated and advanced stage patients, some individual lesions had reduced in size, and others appeared to resolve completely. I was fortunate to present these data at the Innate Killer Summit in San Diego in March and got a lot of very interesting feedback and intrigue from the field. The phase II trial has enrolled patients through Q2 at both intermediate and high doses. Again, analysis of blood samples confirmed the effect of INKmune on increasing NK cell numbers and activation, and crucially, it became apparent that these effects are limited to patients who started with impaired NK function at the time of enrollment. In other words, in this patient group, INKmune only improved dysfunctional NK immunity and did not supercharge NK cells in patients with pre-existing adequate NK function. This is contrary to what we saw in the hematology patients with lymphoma and leukemia. These data allowed us to confirm that two of the most important secondary biomarker endpoints have been met. First, the increased NK cell count following treatment, and second, the increased NK cell function. There was no significant impact on disease burden as measured by PSMA PET. We decided last month to close the trial to recruitment with three patients treated at the low dose, six at the intermediate dose, and five at the highest dose level, and to close the trial after follow-up of the current patient who is on treatment. In general, immunotherapies are best to target minimal residual disease. That's been well known for over 30 years, and that has been our intention with INKmune since its conception. These data showing safety and in vivo NK cell priming potency allow us to move forward in planning a trial in a less advanced patient group, either alone or with suitable partners. That ends my update on the CORDStrom and the INKmune platforms, and I'd like to turn the call back over to David. David? Yeah, thank you, Mark and C.J. Some of you may know Corey Ellspermann, who has been with the company for many years now. He's been a key person in Finance and Accounting and has recently been appointed Interim CFO for INmune. Corey and I have worked together almost since the start of INmune Bio when he was a consultant, and I can tell you, not only do we work incredibly well together, but he is more than capable to take a strong leadership role as Interim CEO. I have full confidence and support in Corey and his ability to help take INmune forward. Now, let me move on to the financials. Net loss attributable to common stockholders for the quarter ended June 30, 2025, was approximately $24.5 million, compared with approximately $9.7 million for the comparable period in 2024. Research and development expense totaled approximately $5.8 million for the quarter ended June 30, 2025, compared with approximately $7.1 million for the comparable period in 2024. General and administrative expenses were approximately $2.3 million for the quarter ended June 30, 2025, compared with approximately $2.8 million for the comparable period in 2024. Impairment of acquired in-process research and development intangible assets was $16.5 million, compared with zero during the comparable period in 2024. Following the release of phase II MINDFuL data, the company has decided to take a very conservative approach and to halt immediate plans to further develop XPro and ED at this time, given the cost of a phase III program as it seeks partnerships. Since we can't guarantee a partnership, we thus took the conservative approach and wrote off the value of XPro's intangible asset value. As of June 30, 2025, the company had cash and cash equivalents of approximately $33.4 million. Based on our current operating plan, we believe our cash is sufficient to fund operations into Q3 of 2026. As of August 7, 2025, the company had approximately 26.6 million shares of common stock outstanding. Now, let me move and talk about some key upcoming milestones. We expect to have the manuscript and the public and the peer-reviewed publication filed on the MINDFuL trial sometime this month, and it should be available to the public as well. We expect to have the end-of-phase II meeting with the FDA to take place sometime in Q4 of this year. As Mark had mentioned, the company is working vigorously on the CORDStrom marketing authorization application and the biologics licensing application to file by mid-year or earlier 2026. In addition, the company expects to have additional CORDStrom data to hopefully share in Q4, as Mark had mentioned earlier. In closing, I want to emphasize that INmune Bio is at a pivotal moment. With CORDStrom, XPro, and INKmune, we have a robust pipeline with clear paths to potential value creation. The recent progress in our programs, combined with the opportunities like the potential extension of the rare pediatric disease Priority Review Voucher program through bills like Create Hope Authorization Act of 2024, position us to capitalize on significant market opportunities. We are committed to executing our strategy with discipline, exploring strategic partnerships to help fuel our growth and complete trials, and deliver therapies that have the potential to transform lives. Your support of shareholders is critical to our success, and I'm confident that together we can achieve great things. Stephanie, at this point, I'd like to turn it over to you to pull for questions. Thank you. At this time, we will open the floor for questions. If you'd like to ask a question, you may press star one on your touch-tone phone now. If you would like to remove yourself from the queue, you may press star two. Again, that is star one if you'd like to ask a question. We'll pause for just a moment to allow questioners to queue. We'll take our first question from Gary Nachman with Raymond James. Hey, guys, this is Denis Reznik on for Gary Nachtman. Congrats on the new role, David, and thanks for taking our questions. You had mentioned that you plan to conduct the end-of-phase II meeting with the FDA in the fourth quarter for XPro. We just want to confirm, has the specific meeting date been set yet? Has there been any changes to anyone you've been previously communicating with at the agency? Can you tell us a little bit more about the atmosphere at the AAIC and what the takeaways were from various thought leaders and KOLs to your presentation there? I've got one follow-up. No, I appreciate that. I'll answer the first question, and then I'll let C.J. talk about AAIC. We have not yet filed the briefing book with the FDA. We're preparing that along with the manuscript, and we expect to have that in soon. As you know, I think there's a 60-day window before you hear about the date. It should fall sometime November, December if we get it in on our target date. That's with regards to the end-of-phase II meeting to the FDA. C.J., you want to discuss the mood at AAIC? Thanks. Some of that I addressed in the script, but to add a little more color to it, I have to say it was even more promising, the feedback than I expected. I think one of the interesting things about it is as we walked through the data, you could see the clinicians and the experts in the field sort of nodding their head as if it was, "Yeah, this is the logical step. Yes, that makes sense. That's how you would proceed." We really didn't get too many questions about the science per se, because at least based on the feedback, it was pretty obvious that this is the appropriate subgroup. It aligns with your hypothesis. These are the endpoints that are expected to change. I think that was really good. One of the things I was perhaps maybe a little surprised about was the real interest in the neuropsychiatric inventory and the potential there. For those of you that aren't familiar, the behavioral changes that occur in Alzheimer's patients are really quite debilitating. As the disease progresses, it's one of those things that really brings patients to the physician's office. It's really not the cognitive decline after a certain period of time. It's quite distressing to both patients and caregivers, not to mention the physicians. To have another option with a differentiated mechanism that can treat the neuropsychiatric symptoms really provides, in some ways, a separate avenue. For it to be also promising as a disease-modifying therapy, I think people were really responding to. Of course, as it relates to the lack of ARIA, despite the fact that most of our patients had high-risk factors associated for developing ARIA, I think that's something that the field is really looking for, especially because combination therapies are where we're going. When you start thinking about putting two therapies together, especially those that potentially have safety signals associated with ARIA, it really stifles that quite a bit. I think those three things were really well received by the community. They understand that the results are appropriate for a phase II study, and it's sort of what you would expect, and it provides a clear path forward. That's really what we're looking for at this stage of development. At least that's what the scientific community is looking for. Really great feedback all around. That was great color. Thank you so much. If I can ask about how the strategic partnerships to accelerate XPro are going, can you just provide some more color about how those conversations are going, what you're specifically looking for in a partner, and what an ideal partnership from a financial perspective looks like to you? Is it likely that you'll have to meet with the FDA for your end-of-phase II meeting before signing the partnership, or could we see a partnership announced before then? Thanks so much, guys. No, I mean, hey, look, that's a very detailed question and smart of you to ask. I don't expect the partnership to occur until after we've had an, if there is going to be one that occurs, until after we've had the end-of-phase II meeting with the FDA. I think that's a critical component. I think the partners are going to want to see the publication. They're going to want to dig into the data, and they're going to want to see what the FDA thinks. Now, keep in mind that depending on who you partner with, most partners are going to have their own regulatory view on how they want to push this through the regulatory process. That could have geographic input as well. I don't suspect that a partnership for XPro is any time in the short period of time. It's going to be more of a long-term type of approach, most likely leading into next year or the first half of next year if it occurs at all. What do we want out of a partnership? You know we believe that XPro can address a major population in Alzheimer's disease with a therapy that's never been addressed before, which is neuroinflammation. If you think about the trial that we ran, it really was an incredibly novel trial. It's something that no one has ever done before, and it's really amongst the first to truly address neuroinflammation. If you think about it, we've always said that the higher levels of neuroinflammation you have, the faster your decline. That showed with whether you had one or two biomarkers, right? We kind of confirmed that in this trial. My belief is that I think everybody knows that there's more and more research coming out about neuroinflammation and neurodegenerative disease, and specifically Alzheimer's. I think that we've got a tremendous amount of data from this phase II program, and the partner we're going to look for is the one that's going to help us get it, be able to help finance a registration trial to get this to approval. How that's structured financially, I couldn't tell you at this point. That's a negotiation to be had. Thanks for all the color, guys. Thank you. We'll take our next question from Thomas Shrader with BTIG. Hi, this is Jenny Kim on for Thomas Shrader. Thank you for taking my question. I wanted to ask about the biomarkers of your trial, particularly in the EMAC, knowing what you do now. Would there be any refinements you made or you would make to measure this marker? For the behavioral marker, MPI, from a registrational point of view, has it been used before in trials or in conversations with the FDA? Thank you. You cut out a little bit. I think I understand. Just to clarify if I don't have this right, you're asking about the EMAC as a biomarker, or are you referring to the true blood biomarkers in relation to EMAC? The EMAC as a marker in general. Okay. Good question. Is the question regarding how we see that as it relates to the FDA or how we would refine our phase II based on the EMAC? Do I have that right? Yeah. Okay. Sorry. I haven't got it clarified. I think, you know, from a performance perspective, the EMAC did what it was supposed to do in the sense that it captured change, that it was sensitive to capture change in these patients. We could see in the placebo group that, you know, that also means that you don't get as much decline. It performed as expected in the right patient population, the patients that had high enough inflammation that did decline. From the pure performance perspective, we were very happy with the performance of the EMAC. We think that the psychometric properties more broadly, so how the test performs as it relates to being able to measure cognitive change in early AD patients, really aligns well with what the FDA has put in their guidance to what a new therapy or a new, I'm sorry, a new scale should look like. I actually am pretty confident that the FDA is going to have a favorable opinion on the EMAC. They do have some things in the guidance, and one of them that I think is less clear and somewhat vague is there has to be scientific consensus around that. It's not clear what that really means. What I can tell you is that there are at least four companies that have used or are using EMAC, including ourselves. There are additional companies that are now going to be looking to put it into the clinical trial. The neuropsych groups that were developing EMAC are at the point of publishing a couple of papers on it. I think that EMAC is going to be well received. It remains to be seen what the decision will be. I feel pretty confident. Does that address the question? I'm sorry, I didn't get that at all. Yeah, that question cut out quite a bit, C.J. I think she was talking about MPI. Yeah, exactly. I think the more up to MPI and whether it would be a good risk for patients. I'm sorry, David. Did you? I think she's cutting out. I'm sorry. I think we're going to have to go to the next question, but I think she was asking something about MPI. Thank you. We'll take our next question from James Molloy with Alliance Global Partners. Hey, guys. Thank you for taking my question. I couldn't hear that question on this end either. On the part, I guess it's probably safe to assume that potential partnership, no one's in the data room yet. It'll be a post-end-of-phase II, the end-of-phase II meeting. Should we anticipate 2026, 2027 potential partnership, again, assuming things go well at the end of phase II with the EMAC endpoint and all that? Yeah, I think that's fair to assume, James. Thank you. We'll go ahead. Okay, great. Any comments from the experts on the EMAC endpoint as well, and their sort of their thoughts? I don't think we've had any detailed discussions about EMAC as an endpoint in a way that would sort of satisfy your question. What I can tell you is that we've had some of the early interests, the quick interests at the AAIC around EMAC as a valid endpoint was really had with the neuropsychs and consultants in the industry that are really interested in that sort of thing. I can tell you that those conversations were extremely supportive. I think, to me, that's a good sign because that's where you develop that scientific consensus. Not a whole lot of, I would say, in-depth conversation with partners. I will say we didn't get pushback. I think that in and of itself is a good sign. Okay, great. Thank you for taking the questions, and best to R.J. and his retirement. Thank you so much. Thank you. We'll take our next question from Boris Tokhachev with Freedom Broker. Good afternoon, and thanks for taking my questions. I'd like to switch gears a bit to CORDStrom. First, regarding the ongoing preparations for the BLA submission, as I understood from the press release, the clinical data are currently undergoing independent statistical analysis. Are you expecting any new insights from that process, or just more of a final quality check to make sure everything's ready for submission? Additionally, could you elaborate a bit on the details of planned open label for the BLA trial of CORDStrom? Is there any intention to eventually include the results of this trial in the BLA package? Thank you. Good question, Boris. Mark? Yes, thanks very much, Boris. First off, the statistical analysis plan that was designed by the sponsor of the crossover trial wasn't really adequate for true detailed analysis of the patient populations. We've looked at that statistical analysis plan and identified great improvements. I do believe that the plan we've put together with Verimed, the independent consultants, is likely to identify significantly improved data that will help our submission both for MAA and BLA. I can't be certain of that because I haven't seen the data. They're blinded to us. I think the analysis plan that we've put together is certainly likely to come up with a more intuitive analysis of data and stronger data to present to the regulators. In terms of the open label, our plan is from our discussions with both the formal discussions with the FDA and informal discussions with the MHRA, we believe that we have data that are adequate from the crossover trial. Bear in mind that this is the first ever fully randomized controlled crossover placebo-controlled trial on multi-center sites done in this patient group anywhere in the world. It's done in the two largest centers in Europe for RDEB, pediatric RDEB. The data really can't be improved upon in terms of patient number. What we expect to do after we've submitted our MAA and BLA applications is to go to look at the open label. The trial protocol is still under negotiation. In fact, I was discussing it with the clinical leads today, looking at that open label. We will move forward probably early 2027 to make certain that those data start to be acquired after we've submitted the BLA submissions. Does that answer your question? Yes, thank you so much. I appreciate the answers. Thank you. No, thank you, David. Thank you. This does conclude our question -and -answer session. I'd like to now turn it back to our presenters for any additional or closing remarks. Thank you, Stephanie, and thank you, everyone, for joining us. INmune Bio has come a long way over the last few years, and we have a very exciting future ahead of us. We thank you greatly for your support and look forward to sharing more accomplishments with you in the near future. Thank you. Thank you, ladies and gentlemen. This does conclude today's presentation. You may now disconnect.