Greetings and welcome to the INmune Bio first quarter 2024 earnings call. At the end of the presentation, there will be a question and answer session. To ask a question, you will need to press star 1 on your telephone keypad. 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. David Moss, CFO of INmune Bio. David? Thank you, James, and good afternoon, everybody. We thank you for joining us for the call for INmune Bio's first quarter 2024 financial results. With me on the call is Dr. RJ Tesi, CEO and co-founder of INmune Bio, and Dr. Mark Lowdell, Chief Scientific Officer and co-founder of INmune Bio, who provide an update on INKmune, our memory-like natural killer cell oncology platform. 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 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 obligations to update these forward-looking statements to reflect future information, events, or circumstances. With that behind us, now I'd like to turn the call over to Dr. RJ Tesi, CEO of INmune Bio. RJ? Thank you, David, and I thank everyone for joining the call. As usual, I will arrange my remarks to highlight the key takeaways from the first quarter and the subsequent period, and provide updates on our platform programs. I will start by reviewing developments in the XPro platform and then pass it over to Mark Lowdell, who will update the INKmune program. David will conclude with the discussion of our financial results, including some commentary around the recent equity capital infusions, and provide an update on upcoming milestones. At a high level, steady progress on all fronts has continued over the last six weeks since we held our fourth quarter conference call in March. We continue to enroll patients globally in our early Phase II trial in Alzheimer's disease called AD02, and we expect to meet our target enrollment by mid-2024. Clinical trial sites continue to enroll patients at a good clip, and we reiterate our commitment to complete enrollment mid-year. I know you want to know the exact date of our last patient enrollment, but we will not predict this because of the vagaries of predicting exact enrollment rates and pace. I promise you that as soon as we enroll that last patient, we will let everyone know. Like you, we eagerly await the conclusion of the Phase II and the corresponding data readout that will occur about six months or so after that last patient is enrolled. Recently, we provided an update on the long-term use of XPro in patients with Alzheimer's disease. In that press release a week ago, we described two patients who participated in the Australian Phase I trial, one with MCI and the other with mild, actually moderate Alzheimer's disease. Both have been taking XPro for roughly three years. Due to the rules of clinical development in Australia, we cannot communicate directly with the patients, but the anecdotes that we received from their treating physicians highlighted the positive impact of XPro on the patient's cognitive health and overall quality of life. If you haven't viewed the video links associated with that press release, I strongly encourage you to do so, as they exemplify what we are trying to achieve with XPro in patients suffering with early AD. Obviously, this is a small sample, but the results speak for themselves. Long-term treatment with XPro in patients with Alzheimer's disease has been shown to be safe, well-tolerated, and made a difference in the lives of these patients and their caregivers. The ongoing blinded, randomized, placebo-controlled trials are a necessary step in the development process, and we believe we are helping these patients, their families, and their caregivers who live with this dreadful disease every day. We want to help you better understand 3 important elements of our ongoing Phase II trial. The elements are duration, size, and primary endpoint. I'll start with the endpoint, primary endpoint. The clinical trial is powered on the cognitive scale called CDR. CDR is a validated endpoint that has been used in the recent Phase III anti-amyloid trials that will all result in approval of those drugs. The endpoint is acceptable to regulatory authorities, certainly in the U.S., and we suspect globally. In our Phase I trial, eight of the nine evaluable patients had stable or better cognition at three months. three of those patients had improved cognition. Two of those were highlighted in the recent press release. This is where we differ a little bit from what the other companies do. We believe some of the patients in ADO2 on XPro will respond like those in the Phase I trial. We need to be able to measure clinical improvement. To do that, we need a better, more sensitive cognitive scale than CDR. And that is why we're using EMACC. EMACC will allow us to accurately determine if patients have improved cognitive function, and we believe that will be an important finding of the Phase II trial. To be clear, the primary endpoint that will be used in the Phase III pivotal trial will come after discussion and after agreement with the regulatory agencies that we work with, including the FDA, EMA, and MHRA. It may be CDR, or it may be EMACC. That decision will be driven by data and the regulatory authorities, not by INmune Bio. The size and duration of ADO2, the Alzheimer's trial, are both smaller and shorter, respectively, compared to the other trials in Alzheimer's disease. This trial design was based on careful analysis of our preclinical data, clinical data, and publicly available databases. First, I want to make a personal statement as a clinician. This is me talking. This is not the company. But when you put a patient into a clinical trial and they get randomized to placebo, we are asking that patient to allow their disease to progress under our care. In my opinion, we need to do everything possible to limit the number of patients who receive placebo and how long they are on that placebo because we're really not benefiting that patient. The ADO2 trial exposes patients to six months of placebo. This is just one-third of the time in the anti-amyloid trials. They were 18 months long. Shorter trials are good for patients, but is it bad for drug development in Alzheimer's disease? The answer is clear. It is not bad for drug development in Alzheimer's disease. ADO2 is fully powered to demonstrate a benefit at 6 months with XPro. In fact, you realize that both the lecanemab and the donanemab trials were statistically positive at 6 months. They could have stopped those trials at 6 months and had the same result that we have today. That is, the drug therapy is better than placebo. There's nothing magical about an 18-month trial or 12-month trial. The issue is statistical power. This is where our unique trial design matters. To our knowledge, ADO2 is the only Alzheimer's trial that uses enrichment criteria to enroll patients. ADO2 enrolls early Alzheimer's patients with biomarkers of inflammation. There is a biologic and statistical advantage to this simple enrollment strategy. The biological advantage is that the mechanism of action of XPro, targeting neuroinflammation, is matched with the patient's disease, that is, the pathology that's driving their cognitive decline. Trials that don't use enrichment gamble that a large number of patients treated for a long time will overcome statistical noise. That's a risky and expensive strategy. The benefits of enrichment are best seen in oncology drug development. Oncology clinical trials routinely use enrichment to de-risk clinical trials. This is called precision medicine. Precision medicine is the standard in clinical oncology drug development, excuse me, it should be the standard in CNS drug development too. We are using a precision medicine approach. The second advantage is statistical, and it's more subtle than this enrichment strategy. Patients with neuroinflammation with Alzheimer's disease progress more quickly and more reliably than patients without neuroinflammation. This is kind of a terrible thing to say, but it's a biologic reality. Put in the language of a statistician who are critical in the design of the trial, the increased delta, the difference between placebo and active and arm, and the lower variance provide important statistical advantages. Overall, the trial is well designed, de-risked, and relevant to today's patients with Alzheimer's disease. To be smart with drug supply and capital resources, we have closed enrollment of the Phase II open label extension. Remember, the open label extension was patients were going to be offered 12 months of therapy in an open label trial as sort of a reward for being in the randomized blinded trial and also to give us additional safety and efficacy data. This was a practical consideration by the company. Having a large patient population on drugs for 12 months consumes both drug and treasure. The first question many ask is, "What will the FDA say?" I remind you, the Phase II trial is not a registration trial. The purpose of the Phase II is to demonstrate safety and efficacy of XPro in the target population, patients with early AD and biomarkers of neuroinflammation. At the end of the Phase II trial, we'll have end-of-Phase II meetings with the regulatory authorities where we will negotiate the design of the Phase III clinical trial. The FDA worries about both safety and efficacy. There's no question the FDA will want more patients treated with XPro who have Alzheimer's disease. The question is, will they want patients treated for a longer period of time? In my mind, the FDA is very focused on doing no harm. That is part of their charter. To ask a patient to be on placebo for 12 or 18 months when they and we already have data to show that you get an effective clinical readout after six months may prove to be an ethical dilemma. At this time, we cannot predict what the FDA will want with the Phase III trial. I predict, and once again, this is R.J. Tesi talking, not INmune Bio, that the FDA will want a larger trial but not necessarily a longer trial. The FDA does provide mechanisms to speed drugs through the development process. The accelerated approval pathways are in place for this purpose. We believe XPro for Alzheimer's disease will qualify for accelerated approval pathway. We will apply for a fast-track approval based on our preclinical and Phase I data. We may be eligible for a breakthrough status after we complete the Phase II clinical trial. We cannot predict how the FDA will respond to our application, but we believe XPro's unique mechanism of action, the importance of neuroinflammation and glial activation in the pathophysiology of Alzheimer's disease, combined with our clinical data, will be a compelling story. Finally, you've heard us talk about the many CNS diseases that XPro can be applied to all that have neuroinflammation as part of their underlying pathophysiology. We have 87 publications on our website with 12 different diseases. This is the future of XPro. It is a CNS franchise in a drug. For now, treatment-resistant depression will be the first disease beyond Alzheimer's disease that we develop. We will have further announcements on the treatment-resistant depression Phase II program using XPro in the near future. Our goal is to enroll that first patient in this NIH-supported Phase II trial in the second half of this year. I will now pass the mic to Mark Lowdell, co-founder and CSO of INmune Bio, to update progress on the INKmune program. Mark? Thanks, RJ, and thanks, everyone, for dialing in. Yes, I'm going to tell you where we've got to with our prostate cancer trial called CaRe-PC. It's unique in many ways, as appears to be typical for our company. First, the concept. This is an NK targeting therapy that doesn't actually administer NK cells or use cytokines, which are the typical historical use of NK targeting therapies. INKmune converts the patient's own NK cells in their circulation and probably actually within their tumor from resting non-cancer-killing state to what we now know are memory-like NK cells that are able to destroy NK-resistant cancer cells. Unlike more conventional adoptive immunotherapies with NK cells from donors, patients don't require any type of preconditioning chemotherapy, nor do they require NK-stimulating cytokines as is common to other NK-activating therapies. The INKmune patients sitting in a chair as an outpatient get an intravenous infusion over about 20 minutes, and then having received their dose of INKmune, they're able to leave. We've given over 20 doses of INKmune in outpatient settings so far. Each infusion has been remarkably boring for the patient and, as importantly, boring for the clinical team because it's been so well tolerated. Each patient in the trial is monitored for immunological endpoints, as you would expect, and these include NK cell number, phenotype of those NK cells, their ability to kill NK-resistant tumor cells. We also measure tumor-related variables. In this metastatic castration-resistant prostate cancer trial, we measure anti-tumor effects by following blood prostate-specific antigen levels, tumor volume with PSMA scans, and we measure circulating tumor DNA. So this rich dataset will allow us to determine whether the drug is ready for a pivotal trial at the end of Phase II. The Phase I Phase II trial is expected to enroll 30 patients. And the men enrolled in CARE-PC have all received previous high-dose therapy but now have metastatic castration-resistant disease. In the trial, they receive three infusions of INKmune, as I said, on an outpatient basis with a six-month follow-up. We have three centers enrolling patients at the moment, a fourth opening this month, and four more are planned to open over the next few months. The Phase I portion of the trial will be completed by September this year, and we expect patient enrollment in the Phase II portion to be completed by the second quarter of next year, with data available for all of the patients by the end of 2025 at the latest. It is an open label trial, which means that we're looking forward to some snapshots of the data in 2024 or early 2025. Equally important as the trial, the INKmune team has been working very hard on perfecting the manufacturing and logistics elements of INKmune for future clinical and commercial development. So I still have a part-time university post, and wearing my academic hat over the last 35 years, I've seen an awful lot of promising therapeutic strategies in the cell and gene therapy space fail due to manufacturing and logistical problems. I'm sure you'll all be aware of some of those associated with adoptive immunotherapies like CAR T cells. We're scaling up the manufacturing process for INKmune in preparation for the pivotal trial, and we've perfected the quality and release assays, which will be required by the regulatory authorities as we move forward. Because the product ships on dry ice, logistics and storage at treatment centers are easy, and they fit with many other commercial drugs. So in summary, we can make the drug, we can quality control release the drug, we can ship it, and hospitals can store the drug. The clinical trials will determine the drug's therapeutic value as we move forward. Our pivot from hematological malignancies to solid tumors was not a one-tumor project, and it's been well planned as an initial transition into the solid tumor space. The unique attributes of INKmune prime NK cells make them ideal to treat a wide variety of solid tumors, and we've published papers on some of those. Prostate cancer is a test case, but we have sound preclinical work in ovarian cancer, and we're developing the same data in renal cell carcinoma at the moment. As we obtain resources, these will be the next targets for INKmune therapy. So that ends my update on the INKmune platform, and I'd like to turn the call over to David Moss, CFO and other co-founder, to discuss the financials. Thank you, 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. However, I'd like to begin with some comments on our recent capital equity raises as we get closer to our Phase II Alzheimer's readout and INKmune data. We are pleased to have raised $14.5 million in gross proceeds from two separate equity offerings over the past weeks at an average price of $8.35 and $9.84 per share. In the two transactions, the company issued an aggregate of approximately 1.5 million shares of common stock and warrants to purchase an aggregate of approximately 1.5 million shares of common stock. The exercise price of the warrants is $9.15 and $9.84, respectively. The warrants are exercisable on the earlier of two-year anniversary of the initial exercise date, or 30 days following the reporting of top-line data in the Phase II Alzheimer's program for XPro. In the first $4.8 million raise, management, employees, and members of the board of directors purchased over $1 million worth of stock. I cannot underscore how financially committed and aligned the entire INmune team is to the success of the company. We greatly appreciate the support from our existing shareholders and the support we saw in both offerings from mostly existing investors, our team here at INmune, but also we welcome a few new holders to the registry. Now moving on to the financials. Net loss attributable to common stockholders for the quarter ended March 31st, 2024, was approximately $11 million compared with approximately $6.5 million for the comparable period as we've reached a scale with both of our clinical programs. Research and development expenses total approximately $8.7 million for the quarter ended March 31st, 2024, compared with approximately $4.1 million for the comparable period. General and administrative expenses was approximately $2.3 million for the quarter ended March 31st, 2024, compared with approximately $2.3 million for the comparable period in 2023. At March 31st, 2024, the company had cash and cash equivalents of approximately $26 million. This figure does not include the recent raises. Based on our current operating plan, we believe our cash is sufficient to fund our operations into 2025. As of May 9th, 2024, the company had approximately 19.8 million shares of common stock outstanding. Now I'd like to focus on some key upcoming milestones. Full enrollment in the Phase II XPro trial for the treatment of neuroinflammation as a cause of Alzheimer's disease are expected mid-2024, followed by top-line data approximately six months from the last patient enrolled. We will initiate a Phase II trial of XPro in patients with treatment-resistant depression in the second half of this year. Last week, we announced completion of cohort one for the first of our three patients taking part in the metastatic castration-resistant prostate program. We expect cohort two to start shortly. We expect complete enrollment in the Phase I portion of the metastatic castration-resistant prostate trial by the end of Q3 2024, and the Phase II portion is expected to complete enrollment Q2 of 2025. Although we've secured additional funding, as always, we continue to focus on achieving our primary clinical objectives while remaining cost-prudent with the potential to recover a portion of R&D expenses in Australia and the U.K. Further, the recent changes RJ mentioned with regards to the open label extension will save the company a couple million dollars in drug and trial-related expenses. In summary, we secured a meaningful equity refinancing recently that puts us in good position heading into data, and our focus remains solely on execution. At this point, I'd like to thank you for your time and attention. I'd like to turn it back to James to poll for questions. James? Thank you, Mr. Moss. At this time, if you'd like to ask a question, please press the star and 1 on your telephone keypad. You may remove yourself from the queue at any time by pressing star 2. Once again, that is star and 1 to ask a question. We'll take our first question today from Tom Shrader with BTIG. Good afternoon. Thanks for taking the question. So RJ, you must be thinking about the role of A beta antibodies in your Phase III. Is there any guidance or thoughts? Are you going to be able to stratify, or could you still do a monotherapy trial? I'm just curious if there's any sort of thought yet. And then a quick one for Mark. I understand, Mark, boring is good, but would you expect some fever if you're turning on NK cells? Just your historical thoughts on why things are so safe. So thanks. Yeah, so let me thank you, Tom, for those. Very interesting question about the anti-amyloid. We have signaled very strongly we are aware that we're going to have to be able to answer the question about combination therapies, and I think we've said that you should expect some preclinical data to that regard from us mid-year. What's more important, though, is how will it affect the Phase III clinical trial? And at least in the United States, the only place these drugs are currently approved, adoption has been slow. So I believe that there will be plenty of patients who are not on the anti-amyloid drugs who will be potential clinical trial participants in the United States. In other regulatory jurisdictions like Europe, U.K., Canada, and beyond, we don't know when those drugs are going to be approved. They'll be approved by the time we start our Phase III, no doubt. But once again, those drugs have had slow adoption, so we are not concerned at this point. We believe a combination trial is actually a different development pathway that may be answering a different question than whether Expo works alone for patients in Alzheimer's with neuroinflammation. David, do you want me to comment on? Is Mark on the phone? I think his call may have dropped. Mark, are you there? Mark? Yes, hello. Mark is on. [crosstalk]. I'll tell you what. Mark got dropped. They'll try and add him back in. He's over in Europe having problems. But in relation to your question, Tom, why you don't see a fever or some sort of inflammatory response, why the drug is so safe, [crosstalk]. So the question was about no fever, why no inflammatory reactions with INKmune. Well, INKmune activates NK cells, and it doesn't activate T cells, and we've spent a lot of time looking at that. So the inflammatory response you see in cytokine release syndrome is entirely T cell mediated, so it's release of inflammatory cytokines from CD4 T cells. And NK cells, which are activated by INKmune or even by cytokines, don't secrete inflammatory cytokines. So no NK therapy itself, and it has been associated with inflammatory-type reactions. Got it. Okay. Thanks for the thoughts on both. No, not at all. It's a very smart question, actually, because it's normally the cytokines that are administered to sustain NK cells that cause side effects. And of course, INKmune doesn't require the administration of cytokines, so it's specifically to NK cell targeting. Got it. Got it. Okay. Thank you. Our next question will come from Joel Beatty with Baird. Hi. Thanks for taking the questions. The first one is for the ongoing Phase II trial in early AD. Could you remind us of the mix of patients you're targeting in enrollment between the ones that have mild cognitive impairment versus mild AD and how enrollment is tracking with that? Yes. Good question. So two things, two points in there. It's relevant considering my comments on placebo. We have a two-to-one enrollment of active to placebo. In other words, for every group of two patients, three patients get Expo, and 1 patient gets placebo. So that's number one. Number two, the way the protocol is written, there will not be more than a two-to-one balance. In other words, although we don't specify whether there's twice as many mild AD as MCI or twice as many MCI as mild AD, it will not be, it will really be an early AD trial like all the other ones do. Statistically, you would expect more MCI patients. But as you recall, we started the trial with only enrolling mild AD patients, so I suspect it will be very close to a 50/50 mix. Don't hold me to that. That's a prediction. But the way it's looking right now, it's going to be about a 50/50 mix. Okay. Great. And then the question on the open label extension study that's, I guess a clarification. Has it just been enrollments that's closed, but some patients in the study are continuing to be dosed, or is dosing complete in all patients? In any case, are there plans to share the open label extension data that you have collected? Yeah. So that's a good question. The open label extension data that we have has always been complicated by the fact that we don't know what the patients were on at entry. Remember, they come into the trial after a blinded randomized trial, so we don't know. So we haven't figured out the best way to analyze those. Right now, because of really, as I said, both drug supply and financial considerations and by the way, drug supply is a financial consideration because making the stuff is not a small task. We are basically working with the sites to decide the best path. Some patients will go onto kind of a scheme where they get compassionate use if that's available to them, and some will be discontinued. The company is not happy with this turn of events, but it is a practical consideration. Our goal and our commitment to investors is to make sure we finish the Phase II trial, get the result we're looking for, and that's where we're focusing our resource. Thank you. Our next question will come from Jason McCarthy with Maxim Group. Thanks for taking the questions. I guess this is RJ's thoughts type of question. RJ, can you kind of opine a little bit on what do you think regulators might want in terms of timing for this trial? So you said that the two approved amyloid drugs, six months, they already saw that they were effective. But given what you know now about markers of inflammation, seemingly FDA willingness to accept correlation between biomarkers and outcomes in Alzheimer's disease, and with any current standard of care in mild or early Alzheimer's, what is the expected rate of decline? Can you really get away with a trial that's just 3-6 months because of all the inflammatory biomarkers that are available that the FDA seems to be more accepting of? So good question, and I'm going to answer it in a series of statements. First of all, I'm not predicting three months. Our trial is six months. threee months is pretty quick. We expect robust results after six months. Now, let's talk a little bit about the biomarkers. Our biomarkers of neuroinflammation in the Phase II trial are enrichment criteria. In other words, they're things you need for enrollment. I'm not convinced that the FDA will accept biomarkers of neuroinflammation as a biomarker of Alzheimer's. What they will accept are biomarkers of what they consider Alzheimer's, which are amyloid, tau, maybe GFAP, which is glial fibrillary acidic protein, a biomarker of astrocytes. Now, the good news is there's very good blood tests for all of those, and I predict that we will actually show a decrease in those biomarkers in the Phase II trial in patients that get Expo. So my bet is that what we've got is we're going to be focused on patients who have neuroinflammation because that's how the drug works. But we don't think that the FDA, we may get surprised, mind you, but we don't think the FDA will actually focus on neuroinflammation as a response. They're going to stick to the biomarkers they know, and they know amyloid and tau, and they might be interested in GFAP, and I don't think they'll be interested in NFL, neurofilament light chains, in Alzheimer's. So those are my predictions. But I really think if we do as well as we think we are, where you've got a placebo group that's racing to really quite significant cognitive impairment, and the XPro group, which is relatively stable, I don't think they're going to force us to treat patients on placebo for a very long time. But they're going to want to see more patients. 200 patients will not be the size of the next trial. It will be at least double that, probably three times that, in my predictions. So from the placebo group, even with acetylcholinesterase inhibitors or something like that, how far out can they go, even with a true placebo effect, and then start to decline? Kind of not fake it till you make it, but you know what I mean, where they will eventually? Yeah. So most of these yeah. So two points. The acetylcholinesterase inhibitors, in general, after three months, certainly after six months, you don't see any benefit with those drugs. Patients have to be on a stable therapy before they can be enrolled, and that's for three months. So any patient that would be enrolled with an acetylcholinesterase inhibitor, donepezil, for instance, would have been on the drug long enough that they are no longer benefiting from the drug. But as you know, many patients are on the drugs, and it's really the doctors are treating themselves as much as they're treating the patients. At least that's my clinical view. I think that the earlier question asked by the Tom Shrader group regarding anti-amyloid is interesting. I don't think the monotherapy trial will not patients won't be on maintenance anti-amyloid. That will be a separate trial and a separate question that we'll ask, hopefully, with a partner that has an anti-amyloid drug because they're the ones who, I think, will be the most curious if the addition of combination therapy may improve both the safety profile of those drugs and the efficacy profile. But that's a question of the future, and the first thing we need to do is prove that the combination is safe in animal models. And as I mentioned, those studies are underway. Got it. Just one quick question on INmune. I think I heard earlier the potential to move towards renal cancer next, depending on resources, of course. But is the selection of renal cancer have similarities to prostate cancer choice in terms of there seems to be a higher proportion of NK cells versus T cells in those tumor types? Absolutely. And so there's a long history. I mean, last week, I was examining a PhD student at the Karolinska who spent four years looking at the same issue. And yes, renal cell cancers are typically heavily infiltrated with NK cells, and there's a prognostic benefit to those patients who have a high NK cell infiltrate. And in fact, there's a negative prognostic effect of having a high CD8 T cell infiltrate. And of course, the drugs that have been approved for renal cell cancer have been NK targeting, Interferon alpha-2. So yes, that's really the rationale behind that, and we've got some very nice data to demonstrate that NK cells do target renal cell carcinoma cell lines better after they've been primed with INKmune. Got it. Thank you, fellas. Our last question will come from Daniel Carlson with Tailwinds Research. Hey, guys. Thanks for taking my question. RJ, you talk about hopefully showing flat on cognition as opposed to steep decline in the placebo group. I'm wondering, if you do put up those type of numbers, is there any chance that conditional approval post Phase II? Yeah. Right. Your lips to God's ears, huh? I do as much as the FDA has tortured us, I do believe, in general, the FDA has their heart in the right place. If the results are extraordinary, and I would consider that an extraordinary result, not only will investors be excited, not only will the company be excited, but the FDA gets excited. Who knows what'll happen, Dan? They will pull out all the stops to help push us along. I don't know what that looks like, but they get excited about groundbreaking data just like you and I do. Is there a chance? Yes. Would I bet more than a steak dinner on it? At this point, no. Man, if we knock it out of the park, I think all bets are off. We'll just have to see what they say. As you know, patient advocacy groups make a big difference with the FDA. The Alzheimer's field or the Alzheimer's advocacy groups, although. There are a lot of patients who are not particularly vocal compared to some of the other indications, which are smaller, such as ALS and DMD. I don't know. It's a great question. I like to dream about it, but I'm not going to hold my breath, Dan. Okay. And just sort of a follow-up on that, what about other jurisdictions? Are they all going to fall in line behind the FDA, or might it get approved on those results elsewhere? I hesitate to ask that question because each of them is a little bit different. And I think the MHRA tends to be one that I think is a little more independent-thinking. The EMA tends to think very much like the FDA. And we certainly haven't seen a lot of regulatory innovation in Alzheimer's disease. But I have to say, some of that is just because they haven't had many swings at the ball, right? For all practical purposes, the only drugs that have come through are the anti-amyloids, and that's kind of a they all look pretty much the same. I don't know. We'll see. And I think that we need, right now, to get this Phase II enrolled, number one. We need to get it analyzed. And then when we see that top-line data, then we'll both have the resources and the insight to move as quickly as we can. And believe me, we'll be making every attempt we can to move quickly. Yeah. So that's great. I look forward to seeing what happens when you ring the bell there. So just one question about TRD. Now that you've got some more capital in, can you just sort of refresh the timeline and get more resources to put there and tell us about this trial and when we can expect something out of it? Expect something out of it. Once again, it's a blind and randomized placebo-controlled trial. So actually getting data, the first thing you're going to hear is that this is the way it'll go. The FDA will announce that the FDA has accepted the IND and the trial is open, first patient enrolled, and then we'll be moving it forward. The speed of the trial will directly be related to how much resources we can put behind it. Right now, the NIH grant only funds about a third of the trial. So we have to be careful because our primary mission, as we've said, is, number one, Alzheimer's, and then, number two, the INKmune CaRe-PC. But we think we'll be able to move that ahead. And as our resources expand, we'll be able to put the pedal to the metal on treating depression. But this year, the two milestones you should hear from, as David said, is that the FDA has allowed us to open the IND because it is a U.S. trial. And the second thing will be the first patient enrolled. That's our goals. And that will conclude today's question-and-answer session. And now I'll turn the conference over to RJ for any additional closing remarks. So thank you. Yeah. With the success of the fundraising, we now have the capital to comfortably complete ADO2, the early Alzheimer's trial, and support CaRe-PC into some of the open-label data in metastatic castration-resistant prostate cancer. Our goal is to provide positive readout in these programs. With positive readouts, we expect we'll be able to access capital markets in a way to allow the company to become more aggressive in pursuing its goals. Both of these products have uses beyond their primary indications, and we believe that with the resources we need given the resources we hope to get, we have the expertise and the team who can capitalize on those other activities, either alone or with partners. For now, we appreciate your support. Thank you very much. This does conclude today's conference call. Thank you for your participation. You may now disconnect.