INmune Bio Inc (INMB) 2024 Q4 法說會逐字稿

Greetings, and welcome to the INmune Bio's 2024 fourth-quarter and full-year earnings call. (Operator Instructions) 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. RJ Tesi, CEO and Co-Founder of INmune Bio, who will provide an update on our clinical programs. Also on the call is Dr. CJ Barnum and Dr. Mark Lowdell, who will be available for Q&A.

Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those such as forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release as well as risk factors in the company's SEC filings, including our most recent quarterly 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. RJ Tesi, who will provide an overview of our clinical programs before I discuss the financials, and we conclude with Q&A. Over to you, RJ.

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 (technical difficulty) 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-risks the trial and improves the probability of success. By integrating inflammatory biomarkers to identify response to patients and utilizing a precise measure of cognitive response, INmune Bio's hope is 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 8 countries. We work 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 possibilities 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 UK, 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 provides INmune Bio with a unique in-licensing opportunity. That is, INmune Bio owns and -- 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 UK, 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 don't 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 that -- in which Professor Anna Martinez reports the responses from the trial that's 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 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 be released. 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 clinical -- 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 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 in 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 has 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 to slow the progressive decline.

We believe the results of this trial will challenge the long-standing plaques-entangled 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 for -- to add to the physicians' armamentarium.

For instance, neuroinflammation plays important roles of 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 inflammaging becomes a reality.

2024 was a major -- 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, RJ. 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 4,145,978 shares of common stock and warrants to purchase an aggregated 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, the management, employees, and members of the Board of Directors demonstrated a 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 31, 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 31, 2024, compared with approximately $20.3 million for 2023.

General and administrative expenses was approximately $9.5 million for the year ended December 31, 2024, compared with approximately $9.6 million for 2023. At December 31, 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 27, 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 R&D expenses in Australia and the UK.

Now I'd like to move on and list our upcoming important milestones. As RJ said, we expect top-line and secondary cognitive endpoints with supportive data from our Phase II XPro trial for the treatment of neuroinflammation that cause of Alzheimer's disease in June. We're very excited this key milestone for INmune Bio is now less than 100 days away from clinical readout.

We have 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 will enroll six additional patients in each of the middle- and high-dose cohorts. We expect to complete enrollment of the trial as it's currently designed by the end of '25, 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 [miracle] 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 read out, 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. RJ will have some concluding comments. Margo, can you please poll for questions?

(Operator Instructions)

George Farmer, Scotia Bank.

Hi. Good afternoon. Thanks for taking my questions. A couple for 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? And are there different requirements, do you think, for FDA approval and UK approval?

Mark, do you want to handle that?

Yes. 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 1. And those are data that the FDA has 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, and I can't predetermine what the FDA will say, but they did not tell us that we would not be eligible for a BLA.

So we're working towards that, and we are doing the 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 didn't 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.

So at the moment, the answer is we are waiting 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. And we will plan to do that trial both in the US and in the UK.

Okay. Thanks. And then on XPro, I assume we've talked about how you intend to release the data in June, and thanks for the clarity, RJ. 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? And is that still how you're thinking about communicating the top line?

CJ?

Yeah. Thanks for the question. So what we're going to be able to do is we're going to provide cognitive and functional evidence. So all the assessments that assess both cognition and function will be available at the time of release.

We have not said that before, 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. So we will have all those clinical endpoints available in June.

George, that means both EMACC and CDR will be released when the data becomes public.

[Paul Rader], BTIG.

Is that me, Paul Rader?

I think that's --

That's Tom Schrader, right? (multiple speakers)

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 100 days of your lives, but I don't know.

Just remind us where the FDA is on EMACC. 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?

And then just a clarification, you said you'd screened 800. That was 800 after they were already neuro or inflamed? Or is that 800 total?

And then 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.

Thanks. Let me take the last one first. So 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. So 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. But what we've done is we've made sure that we followed 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. And as you know, I'm always surprised by what the FDA says. So I think that's something to be aware of. And I forgot the third question.

The screen failure question. Yeah.

So we're going to have a poster that describes that next week. So I won't give too much detail because that information is embargoed. But 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.

And 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%. And that was obviously a concern of ours is what would happen when we sort of superimpose inflammation on that? Would we see more screen failures? And the answer is no. And I think that's a testament to the fact that most of these patients that have Alzheimer's disease actually have underlying inflammation. So I think that's a good thing.

If I can just add -- reinforce what CJ said that next week is AD/PD, which is the largest Alzheimer's meeting in Europe, and we have a poster that was accepted that discusses, shall we say, the profile of the patients that were enrolled. And you'll see a press around that and then a link to the poster, I think, on Wednesday or Thursday. So 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.

And Tom, one last thing is I encourage you to go back and look at the EMACC webinar, because there's actually -- 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.

Gary Nachman, Raymond James.

Hey, guys. Good afternoon. This is Denis Reznik on for Gary Nachman. Congrats on all the progress. So first, on the EXPAREL Phase II trial, are you aware of any dropouts occurring? And if they are occurring, is it in the range that you were expecting? And what might be some of the main reasons behind those dropouts?

And then 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? And then any additional color as to what a Phase III could look like in terms of the amount of patients being enrolled, duration, and the endpoints you consider? And then I've got one follow-up.

Yeah. So 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? And the answer is no. We account for that. And 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. So 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. So I think that's a good thing.

And the second thing regarding a Phase III 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. 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. So I think there's so much that's 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 or they may say, no, we want you to do the CDR, and we may have to power it differently. So I think what the trial is going to look like, what it's going to cost, and when we can start is really going to be dependent on that conversation with the FDA. But 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. And then just 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, and congrats on all the progress.

Go ahead, David.

Yeah. I'll jump in. That's great question. I think it's actually probably also priced with XPro. We always say you never build a company for acquisition; you build 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 don't necessarily want to recreate that wheel. But at this point, we're 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'll be a lot more interest in what we're doing.

Same thing goes for XPro, right? I mean we're working to get to a Phase III program. I do believe that if we have the accomplishments that we all believe we're going to have, there'll be a lot of interested parties. And again, we don't want to recreate the wheel in drug distribution and so on. But we're 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.

Elemer Piros, Rodman.

I think all of my AD-related questions were answered. So thank you. But 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 UK and in the US and probably in the early part of 2026?

Mark?

Yes, that's true. The team in the UK manufactures and does all the process development and regulatory filing for both INKmune and CORDStrom. And so now that INKmune -- all of the drug is made to complete the Phase II trial, that team is swinging entirely into CORDStrom, and we are appointing additional staff. So 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.

But yes, we expect to have all of those questions answered, all of the data ready for us filing, as David said, in the first half and the first quarter of 2025. And those staff posts are being filled at the very moment.

So 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. And maybe just a little follow-up there. But you are able to start the open-label extension trial earlier than next year?

Yes. So the open-label trial in the UK is ready to go. We already have the first doses manufactured, and that's 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 US, and that's subject to the funding environment which we live. But yes, we have an IND planned for the US, and the CTA is already approved in the UK.

James Molloy, Alliance Global Partners.

Hey, guys. Thanks very much for taking my question. I had a question on the CORDStrom platform with the BLA coming in the first quarter '26 run-up. Any issues with getting under the wire of the PRV program being granted? And any thoughts on what's going on with the PRV that's going to be renewed?

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. And the reason I think it gets extended is because truly, there's no cost at all to the US government. They're very obviously focused on cutting costs. And 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.

So 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'd probably know, by the way, before the end of this year, if it gets extended or not, and we'll plan accordingly. But 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. So we're really going to spend a lot of time on the quality of these applications.

I'd like to now turn the call back over to Dr. RJ Tesi for closing remarks.

So we are busy. It's heads down at INmune Bio as we get ever closer to our important readout in AD02. But 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're well-designed, and we execute them with care.

But as far as AD02 goes in 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 a 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. And ladies and gentlemen, that does conclude today's conference. We appreciate your participation, and you may disconnect at any time.