As a reminder, this conference is being recorded, and a transcript will follow within 24 hours of this conference call. At this time, it is now my pleasure to introduce Mr. David Moss, CFO of INmune Bio. David? Thank you, Margo, and good afternoon, everyone. We thank you for joining us for the call for INmune Bio's 2024 fourth quarter and full year financial results. With me on the call today is Dr. R.J. Tesi, CEO and Co-founder of INmune Bio, who will provide an update on our clinical programs. Also on the call is Dr. C.J. Barnum and Dr. Mark Lowdell, who will be available for Q&A. Before we begin, 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 filing 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 to 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 obligations to update these forward-looking statements to reflect future information, events, or circumstances. With that behind us, at this time, I'd like to turn the call over to Dr. R.J. Tesi, who will provide an overview of our clinical programs before I discuss the financials, and we conclude with Q&A. Over to you, R.J. Thank you, David, and thank you to everyone joining our call. These are exciting times at INmune Bio. 2024 was a transitional year for our company. We believe this year will be a transformational year. In less than 100 days, we expect to announce top-line data for our randomized blinded placebo-controlled phase II trial using XPro to treat patients with early AD with inflammation. We call the trial AD02 or MINDFuL. We have worked tirelessly to get to this point, and I must say hats off to the entire team at INmune Bio for reaching this major milestone. We can't wait to learn the results. INmune Bio's AD02 Alzheimer's trial stands out from conventional approaches of treating Alzheimer's disease due to a focus on treating neuroinflammation as the primary driver of the disease. Rather than targeting plaques and tangles, the dominant traditional targets of Alzheimer's drug development, we have targeted inflammation as the main driver. Because of the frustrating history of failed trials to treat Alzheimer's disease, we adopted a precision medicine approach for our phase II program. That precision is first seen in patient selection. The AD02 trial uses clinical biomarkers to match the patient's pathophysiology with XPro's mechanism of action. That is, XPro targets neuroinflammation. Therefore, we enriched the trial with 80 patients who have neuroinflammation driving their Alzheimer's disease. To our knowledge, AD02 remains the only Alzheimer's trial using biomarkers other than amyloid or tau to guide patient selection. Next, we embraced EMACC as the primary endpoint of the trial. EMACC is designed to accurately test cognitive function in patients with early Alzheimer's disease. We don't understand why others embrace the use of cognitive tests designed for staging patients with Alzheimer's disease or developed for use in patients with moderate to severe Alzheimer's disease as the primary endpoints for studies in patients with early Alzheimer's disease. Those measures of cognition are not designed to measure the clinical effectiveness of a therapy. EMACC is a purpose-built, objective test of cognitive function designed to be used in patients with early Alzheimer's disease with a dynamic range that allows the measure of worsening and improving cognitive function. Although the term precision medicine is most often used to define patient selection criteria in clinical trials, we believe EMACC provides a precision medicine measure to efficacy in Alzheimer's trials. The embrace of these novel approaches is based on solid preclinical data, compelling phase I data, and a belief that addressing the structural and pharmacological aspects of protocol design de-risk the trial and improve the probability of success. By integrating inflammatory biomarkers to identify response of patients and utilizing a precise measure of cognitive response, INmune Bio's hopes to do more than just slow cognitive decline. Our goal is to stop cognitive decline. If successful, we will challenge the long-standing amyloid-centric paradigm of Alzheimer's disease while supporting the perspective that Alzheimer's is an immunologic disease. Today, we are less than 100 days away from reporting the results of AD02. The trial enrolled 208 patients in eight countries. We worked to enroll the right patients into the trial, which resulted in us screening nearly 800 patients. This seemingly simple process of patient screening was time-consuming, complicated, and expensive, but one of the four important drivers of success in AD02. The second and third drivers are the previously mentioned enrichment criteria used to select patients with neuroinflammation and the use of EMACC to precisely assess cognitive response. The final driver is XPro, the drug. Success of this drug in patients with dementia caused by neuroinflammation may open a world of possibility for patients with neurologic disease because neuroinflammation is a common denominator in many difficult-to-treat CNS diseases. Also, in 2024, we completed the pivot to solid tumors with INKmune, our NK cell targeting platform. Although INKmune had interesting data in the treatment of hematologic diseases, we believe the future opportunities for INKmune were greater by targeting and treating solid tumors. The CaRe PC trial using INKmune to treat men with castrate-resistant metastatic prostate cancers has made steady progress. We recently announced completion of dosing in the phase I dose escalation part of the phase I/II trial and continue to dose patients in the phase II part of the trial at the medium and high dose cohorts. As currently designed, we expect to complete dosing of patients with INKmune during 2025, and we have promised that as data become available in those cohorts, because it is an open-label trial, we will report it. CORDStrom is a 2025 event, but in fact, CORDStrom has been a quiet part of INmune Bio since 2018. Dr. Mark Lowdell invented and perfected CORDStrom to support an NIHR-funded trial in the U.K. treating kids with intermediate to severe recessive dystrophic epidermolysis bullosa, or RDEB. RDEB is a rare genetic disease caused by the mutation of the COL7A1 gene. The NIHR is the research arm of the United Kingdom's National Health Service. The INmune Bio team saw the clinical data on the use of CORDStrom in kids with RDEB for the first time in November of 2024. The data are compelling and provide INmune Bio with a unique in-licensing opportunity. That is, INmune Bio invented and owns CORDStrom, the drug, and GOSH, which is the Great Ormond Street Hospital for Children, which is the largest pediatric hospital in the U.K., was the sponsor of the clinical trial and owned the Mission EB clinical data. Mission EB is the name of the clinical trial that was performed at GOSH. Combining the two assets was necessary to generate value to the patients, caregivers, and investors. INmune Bio in-licensed the Mission EB clinical data, resulting in what we believe is a BLA-ready program that has already been awarded orphan drug status and rare pediatric disease designation. CORDStrom differentiates itself from other approved therapies for RDEB by providing a systemic disease-modifying approach rather than focusing on local wound management. Many of you know that the wounds that do not heal are one of the major problems of this debilitating disease. We are not discounting the importance of those therapies, but RDEB affects every organ system in the body except the brain. Topical wound therapies, while providing important local benefits, do not address problems in the eyes, problems eating, and elsewhere in the body. These many problems require systemic disease-modifying therapy. CORDStrom is an allogeneic pooled umbilical cord-derived mesenchymal stromal cell platform delivered intravenously. CORDStrom is a systemic therapy that aims to modulate inflammation, promote wound healing, reduce the debilitating itch, pain, and scarring that exacerbate RDEB in the skin, the esophagus, the eyes, and beyond. The patient caregiver interviews provide some of the most interesting information or data from the blinded randomized Mission EB trial. Those are best heard by listening to the webinar in which Professor Anna Martinez reports the responses from the trial that is available on our website. The impact of CORDStrom therapy on patients' quality of life seems clear. We believe this program is on a rapid path to the market where it will fulfill an unmet clinical need in kids with this desperately debilitating and ultimately lethal disease. While we love our cell therapy programs, we understand that AD02 top-line data is the catalyst everyone, including ourselves, are looking forward to in the near term. At our core, INmune Bio is a CNS company focused on Alzheimer's disease. We have built this company around our XPro platform and are now less than 100 days away from the results of the trial in the phase II trial in Alzheimer's patients with biomarkers of inflammation. I reiterate, we will provide top-line results for the trial in June. I don't know exactly what date in June the top-line data will release. There are too many moving parts, but it will be June. Also, there is no industry-wide definition of what top-line data means. Our definition is simple. The data will provide unequivocal evidence of the impact of XPro on the treatment and the response of those clinical symptoms of patients with early Alzheimer's disease with biomarkers of inflammation. This means we will provide a robust package of cognitive, clinical, and functional data from patients treated with XPro in the trial. From these data, we will provide an answer to the question, does treating early Alzheimer's disease in patients with biomarkers of inflammation with XPro safely alter the trajectory of their cognitive decline? There are four important aspects in the statement I just made. The trial is in early AD. We are not studying patients with moderate or severe disease. Early AD patients are the same group that virtually everyone studies, including the approved anti-amyloid drugs. We are enrolling patients with biomarkers of inflammation. That is, this is not an all-comers trial, but a precision medicine trial enriched with early Alzheimer's patients that have neuroinflammation. Three of the four enrichment criteria are biomarkers of peripheral inflammation, not central inflammation. This first makes them easy to obtain in peripheral blood, but importantly, experts agree that peripheral inflammation causes central inflammation that drives the Alzheimer's disease. Because XPro treats both peripheral and central inflammation, it should stop disease in the brain and eliminate the fuel that feeds progression of the disease. Safety is paramount when treating elderly patients with Alzheimer's. As of today, there have been no unscheduled neuroimaging studies, no emergency MRIs. There have been no deaths, and the number of infections can be treated on one hand. This is a remarkable history in a group of patients that averages 73 years old. Thus far, XPro is shown to be safe in that target population. Finally, I chose the word trajectory of their cognitive decline carefully. Currently, approved therapies slow the rate of cognitive decline, and realistically, we need to be as good as the currently approved therapies to claim success, but we have higher aspirations. Our goal is to halt disease progression or halt cognitive decline rather than slow the progressive decline. We believe the results of this trial will challenge the long-standing plaques and tangles disease paradigm of Alzheimer's disease, providing a fresh perspective on the treatment of Alzheimer's disease as an immunologic disease. We hope the first day of XPro therapy is the last day of cognitive decline in patients with early AD. We will know soon if this lofty aspiration is realized. We are confident. While we remain very optimistic about the upcoming results from AD02, we believe bigger changes are afoot. Positive results will create a paradigm shift for the treatment of Alzheimer's disease and other CNS diseases where neuroinflammation, often ignored and untreated, is finally recognized as an element of many of these diseases, and we now have a tool to add to the physician's armamentarium. For instance, neuroinflammation plays important roles in dementia associated with FTD, Parkinson's disease, traumatic brain injury, stroke, depression, and beyond. Chronic inflammation is the driver of many diseases of aging, and if we achieve our expected results, targeting the immune dysfunction of inflammation becomes a reality. 2024 was a year of major accomplishments in all our programs. Great progress was made in the clinic with our legacy programs. The addition of CORDStrom has added a third therapeutic platform to the company that should accelerate our timeline to becoming a commercial entity. I turn it back to David to go over the financials. Thank you, R.J. As usual, I'll provide a brief overview of our financial results and upcoming milestones before we head to Q&A. During 2024, we raised $29.9 million from the sale of common stock and warrants for cash. In total, the company issued an aggregate of 4,145,978 shares of common stock and warrants to purchase an aggregate 3,898,852 shares of common stock. Term of the warrants issued in 2024 may be accelerated with positive AD02 data as defined in the warrant agreements, which, if exercised for cash, will raise additional capital to the company. I note that with close to 4 million warrants issued and the ability to accelerate as stated in the filings, this could potentially raise approximately $30 million. In the financings, management, employees, and members of the board of directors demonstrated strong participation. I cannot underscore how financially committed and aligned the entire INmune Team is to the success of the company. We also greatly appreciate the support we saw in the offering from both new and existing investors, along with our team here at INmune Bio. We thank our shareholders who have stuck with us during a very volatile time in drug development. Net loss attributable to common stockholders for the year ended December 31st, 2024, was approximately $42.1 million, compared to approximately $30 million for 2023. Research and development expenses totaled approximately $33.2 million for the year ended December 31st, 2024, compared with approximately $20.3 million for 2023. General and administrative expenses were approximately $9.5 million for the year ended December 31st, 2024, compared with approximately $9.6 million for 2023. At December 31st, 2024, the company had cash and cash equivalents of approximately $20.9 million. Since year-end, we've raised an additional $5.4 million through the use of the ATM. Based on our current operating plan, we believe our cash is sufficient to fund our operations through Q3, not including any R&D rebates, exercise of warrants, or any financings. As of March 27th, 2025, the company had approximately 22.9 million shares of common stock outstanding. We continue to focus on achieving our primary clinical objectives while remaining cost-prudent with the potential to recover a portion of our R&D expenses in Australia and the U.K. Now I'd like to move on and list our upcoming important milestones. As R.J. said, we expect top-line and secondary cognitive endpoints with supporting data from our phase II XPro trial for the treatment of neuroinflammation that caused Alzheimer's disease in June. We're very excited that this key milestone for INmune Bio is now less than 100 days away from clinical readout. We've completed all three cohorts of the metastatic castration-resistant prostate cancer program. We have now moved on to phase II of the trial, in which we'll enroll six additional patients in each of the middle and high-dose cohorts. We expect the complete enrollment of the trial as it's currently designed by the end of 2025, and data in the trial will be released as it becomes available later this year. Finally, we expect to file a BLA for CORDStrom in RDEB sometime in the first quarter of next year. This is a seminal event for the company. If approved, it would be our first marketable therapeutic and transition us to a revenue-generating company, a major milestone for any biotech. I'd like to reiterate that we're incredibly proud of our team for navigating a difficult environment to get to this point of less than 100 days to readout, in which we believe could be a major milestone for patients and their families with Alzheimer's disease. When I say team, this not only includes our incredible coworkers, but also our shareholders who have taken the time to properly understand our scientific approach. Great companies, as we like to say, are built when management thinks like shareholders and investors, and investors, shareholders think like management. At this time, I'd like to turn the call back to the operator for Q&A, Margo, and then we'll conclude. R.J. will have some concluding comments. Margo, can you please poll for questions? Thank you so much. As a reminder, ladies and gentlemen, if you would like to ask a question, please press the star one on your telephone keypads. You may remove yourself from the queue at any time by pressing star two. Again, that is star one for a question. While we build that queue, we'll take our first question from George Farmer with Scotiabank. Please go ahead. Hi. Good afternoon. Thanks for taking my questions. A couple from me regarding the RDEB program. It says in the press release you're doing this 12-month open label trial. Is that required for filing? Are there different requirements, do you think, for FDA approval and U.K. approval? Mark, you want to handle that? Yes. We're gathering the, as I think we said in February, we now have access to all of the clinical data from the current trial, Mission EB part one, and those are the data that the FDA have seen. We spoke to the FDA in that discussion about this being adequate for a BLA, and we still believe that it will be. Obviously, that's a decision the FDA will take, so I can't predetermine what the FDA will say, but they did not tell us that we would not be eligible for a BLA. We are working towards that, and we are doing a considerable amount of work, not just on the data analysis as the data are made more available to us, but also in developing the rest of the database that will be needed to submit a BLA with respect to the understanding of the product, manufacturing, and all of the rest of those data. In terms of the MHRA, they approved the trial initially as a, well, they did not approve it, but it went to them initially as a registration trial, and we expect to be able to share the data with the MHRA and get a formal opinion on that early next year. They will also want to see the CMC data that we have to put together with it. At the moment, the answer is we're waiting to hear, we will wait to hear from regulators when we're able to show them the data that we have. We still intend to go ahead with the open label because it tells us an awful lot more about the persistence of the effects and the best way to deliver the drug in terms of the number of repeat treatments and the timing of those repeat treatments. We will plan to do that trial both in the U.S. and in the U.K. Okay. Thanks. And then on XPro, I think we've talked about how you intend to release the data in June. Thanks for the clarity, R.J. There is the EMACC endpoint, but there's also the CDR endpoint, and I believe you said that those results would be staggered. Is that correct? Is that still how you're thinking about communicating the top-line results? C.J.? Yeah. Thanks for the question. What we're going to be able to do is we're going to provide cognitive and functional evidence. All the assessments that assess both cognition and function will be available at the time of release. We have not said that before. We We wanted to make sure that we could do all those things, and we've worked really hard with our vendors to make sure that we have the data cleaned, we have the data analyzed so that you're getting the most accurate data at the time. We will have all those clinical endpoints available in June. George, that means both EMACC and CDR will be released at the same time when the data becomes public. Okay. Thanks, R.J. We'll next go to Paul Rader with BTIG. Please go ahead. Is that me, Paul Rader? No. I think that's— It's Tom. That's you, Tom. That's Tom Shrader, actually. We knew who it was by the last name. Go ahead, Tom. I thought I'd been fired. Anyways, good luck. It's going to be the longest hungry 100 days of your lives, but I don't know. It is. Just remind us where the FDA is on EMACCs. Is a lot of the acceptance going to come from this trial if it aligns closely with CDR, or do you think the FDA is already there? Just a clarification, you said you'd screened 800. That was 800 after they were already inflamed, or is that 800 total? One quick follow-up on— C.J.? If I could ask a quick follow-up on TRD, do all the same cuts in patients there make sense? Will it be peripheral inflammation? Is that going to be basically the same enriched population? Thanks. C.J., if you— I'll take the last— Yeah. Let me take the last one first. They are enriched. We're using CRP, and we're using a behavioral marker of enrichment of anhedonia that is tied really closely to not only peripheral inflammation, but the biological response to inflammation, which is this sort of functional disconnectivity within the CNS, and we can talk more about that. Similar, but a little bit different, and it's really based more on the disease specifics. Regarding EMACC, the FDA doesn't comment on it until they see the data. Their comment is always, "Let us see the data." What we've done is we've made sure that we follow their— and I think we've said this before— they have a playbook. We've followed it, and we think we've got as good a chance as any to get them to agree to it. We don't see too many holes, but I also don't know what they're thinking. As you know, I'm always surprised by what the FDA says. I think that's something to be aware of. I forgot the third question. The screen failure question. Yeah. We're going to have a poster that describes that next week. I won't give too much detail because that information is embargoed. I will say that, no, the screening is not a function of the inflammatory biomarker. In fact, the screen failure due to the inflammatory biomarker is very low on the list. It's actually less than 10% of patients that didn't make it. Most of them didn't make it because of more typical things like diagnosis and that sort of thing. The screen failure rate, which is about 72%, is really spot on compared to what you see with all the other AD trials, somewhere around 70%, mid 70%. That was obviously a concern of ours is what would happen when we sort of superimpose inflammation on it. Would we see more screen failures? The answer is no. I think that's a testament to the fact that most of these patients that have Alzheimer's disease actually have underlying inflammation. I think that's a good thing. Yeah. If I can just add, reinforce what C.J. said, that next week is AD/PD, which is the largest Alzheimer's meeting in Europe. We have a poster that was accepted that discusses, shall we say, the profile of the patients that were enrolled. You'll see a presser on that and then a link to the poster, I think, on Wednesday or Thursday. I encourage you to look at it because it's kind of fun reading because you've been hearing about it for a couple of years, and you'll see what the actual data are. Tom, one last thing is I encourage you to go back and look at the EMACC webinar because there's actually a—Sarah Barnum actually goes over the variables that the FDA requires for approval with EMACC, and she highlights all of the key criteria and what we've done to meet them. It's actually worth your time. Great. Thank you. Next, we'll go to Gary Nachman with Raymond James. Please go ahead. Hey, guys. Good afternoon. This is Denis Reznik on for Gary Nachman. Thanks for taking the questions and congrats on all the progress. First, on the XPro phase II trial, are you aware of any dropouts occurring? If they are occurring, is it in the range that you were expecting? What might be some of the main reasons behind those dropouts? If you think a little bit further down the line, assuming positive results that suggest progressing this asset forward, how soon could you start a phase III trial? Any additional colors to what a phase III could look like in terms of the amount of patients being enrolled, duration, and the endpoints you'd consider? I've got one follow-up. All right. C.J., start with the dropout. Yeah. I think the spirit of your question, if I'm wrong, please correct me, is are we concerned that there's too many patients dropped out that we're not going to have enough power? The answer is no. We account for that. I would say that I don't know the exact number off the top of my head, but it's less than what we expected. The most common reason for dropouts, quite honestly, is just what you get with elderly patients. We're not seeing anything that indicates patients are dropping out at a high rate due to a potential drug efficacy or safety impact. It's mostly just elderly-related issues. I think that's a good thing. The second thing regarding a phase II trial, I don't know how to answer that. I think a lot of it depends on the data. It depends on the discussion with the FDA. I mean, we may see incredible results that suggest we could power a study with 150 patients. The FDA may come back and say, "No, you need a larger safety database. We want 1,000 patients." I think there is so much that is up in the air. I think it also depends on whether or not they like the EMACC. They may say, "Yeah, great. Do the EMACC, then we can do fewer patients." They may say, "No, we want you to do the CDR," and we may have to power it differently. I think what the trial is going to look like, what it is going to cost, and when we can start is really going to be dependent on that conversation with the FDA. The expectation is we're going to move as fast as we can to get it going very quickly. That's very helpful. Thank you. I know it's still early, but on the potential commercial launch of CORDStrom, what's your current thinking about how you plan to commercialize that? Would that be by yourself, or would you look for a partner for that? Thanks so much, guys. Congrats on all the progress. Go ahead, David. Yeah. I'll jump in. That's a great question. I think that's actually probably also a surprise with XPro. We always say you never build a company for acquisition. You build it to be standalone. Our goal is to really move it forward to get it to commercialization. I do fully expect we will probably get a partner when it gets that close just because we are not distribution experts or marketing experts, and we do not necessarily want to recreate that wheel. At this point, we are really heads down on focusing on getting that regulatory document in so that we can get to that point. Once we get close, I think there will be a lot more interest in what we are doing. Same thing goes for XPro, right? I mean, we are working to get to a phase III program. I do believe that if we have the accomplishments that we all believe we are going to have, there will be a lot of interested parties. We do not want to recreate the wheel in drug distribution and so on. We are prepared to go it alone if we have to. I doubt that will be the case. I'll also say that when it comes to partnerships and when it comes to M&A or whatever it may be, we have pretty lofty goals if we're successful, and we want to make sure if it's done, it's done right. Thanks so much. Perfect. Next, we'll go to Elemer Piros with Rodman. Please go ahead. I think all of my AD-related questions were answered, so thank you. I just wanted to clarify on the RDEB program. Did I understand correctly that you would need the balance of the year to complete the CMC and actually consider filing both in the U.K. and in the U.S. and probably in the early part of 2026? Mark? Yes. Yes. Yes, that's true. The team in the U.K. manufactures and does all the process development and regulatory filing for both INmune and CORDStrom. Now that all of the drug is made to complete the phase II trial, that team is swinging entirely into CORDStrom, and we're appointing additional staff. It will take us until the end of the year to get the answers to some of the questions that the FDA raised in our last filing. Yes, we expect to have all of those questions answered, all of the data ready for U.S. filing, as David said, in the first half and the first quarter of 2025. Those staff posts are being filled at the very moment. Yes, those data are ongoing, and we will have those data ready. We're also looking at a third party to do an external review of the data that we have and to do a gap analysis and inform us from their regulatory expertise that we will be ready by the end of Q1 next year. Thank you. Maybe just a little follow-up there. You are able to start the open-label extension trial earlier than next year. Yes. The open-label trial in the U.K. is ready to go. We already have the first doses manufactured, and that is subject to Great Ormond Street being ready to open. We are currently putting together the paperwork for an IND to open a parallel trial in the U.S., and that is subject to the funding environment in which we live. Yes, we have an IND plan for the U.S., and the CTA is already approved in the U.K. Thank you. Thank you very much. Our last question comes from James Molloy with Alliance Global Partners. Hey, guys. Thanks very much for taking my questions. I had a question on the CORDStrom platform with the BLA coming in the first quarter of 2026. Do Do you run up into any issues with getting under the wire for the PRV program being granted? Any thoughts on what's going on with the PRV that's going to be renewed in there? Yeah. Hey, Jim, I'll just jump in. I'll leave that to David. Yeah. No, Jim, I appreciate it. Look, if we get it in, it's about a six-month process since we have ODD designation already. We're working as quickly and diligently as we can to make that. The deadline is really the end of September for approval. My guess is that program gets extended. The reason I think it gets extended is because truly there's no cost at all to the U.S. government. They're very obviously focused on cutting costs. This program actually provides no cost. It provides benefit. In fact, I think it's very clear to them that because of the PRV program, it's one of the reasons why there is so much ultra-rare and rare disease drug development. I cannot see the rare disease programs necessarily going forward that are small unless they have a program like this in place. I really see no reason why it doesn't get extended, but we're planning just in case it doesn't. My guess is we probably know, by the way, before the end of this year if it gets extended or not, and we'll plan accordingly. Our goal, as we did with the INKmune submission, the INKmune IND, is to do one submission and try and get it through in one pass. We are really going to spend a lot of time on the quality of these applications. All right. Great. Thank you for taking my questions. I would like to now turn the call back over to Dr. R.J. Tesi for closing remarks. We are busy. It is heads down at INmune Bio as we get ever closer to our important readout in AD02. As a three-platform company, we have not taken our eye off our cell therapy programs, which are pretty exciting and quite novel. We are confident in these programs because we have compelling science, excellent drugs. When we do clinical trials, they are well-designed, and we execute them with care. As far as AD02 goes and Alzheimer's, the idea that inflammation and immune dysfunction are drivers of this awful disease is no longer considered novel by the scientific and biopharma community. We believe INmune Bio is the leader in this neuroinflammation space and look forward to presenting our data to the world in June. These are exciting times, and we greatly appreciate our committed shareholder base, and we thank them for investing alongside us as we work to achieve our goals. Thank you very much. Thank you. Ladies and gentlemen, that does conclude today's conference. We appreciate your participation, and you may disconnect at any time.