INmune Bio, Inc. (NASDAQ:INMB) Q4 2024 Earnings Call Transcript

INmune Bio, Inc. (NASDAQ:INMB) Q4 2024 Earnings Call Transcript March 27, 2025

INmune Bio, Inc. beats earnings expectations. Reported EPS is $-0.4, expectations were $-0.54.

Operator: Greetings, and welcome to the INmune Bio’s. 2024 Fourth Quarter and Full Year Earnings Call. At this time, all participants are in a listen-only mode. [Operator Instructions]. As a reminder, this conference is being recorded, and the 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?

David Moss : 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 the risk factors in the company’s SEC filings, including our most recent quarter filing with the SEC. There’s no assurance of any specific outcome. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances. With that behind us, 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 will conclude with Q&A.

Over to you RJ.

Raymond Tesi: 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 a hundred days, we expect to announce top-line data for our randomized, blinded, placebo-controlled Phase 2 trial using XPro to treat patients with early AD with inflammation. We call the trial ADO2 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 ADO2 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 2 program, that precision is first seen in patient selection. The ADO2 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, ADO2 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 test designed for staging patients with Alzheimer’s disease or develop 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 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 derisk the trial and improve the probability of success. By integrating inflammatory biomarkers to identify response to 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 longstanding amyloid-centric paradigm of Alzheimer’s disease while supporting the perspective that Alzheimer’s is an immunologic disease. Today, we are less than one hundred days away from reporting the results of ADO2. The trial enrolled 208 patients in eight countries.

We worked to enroll the right patients into the trial, which resulted in enough screening nearly 800 patients. This seemingly simple process of patient screening is time was time-consuming, complicated and expensive, but one of the four important drivers of success in ADO2. 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 EXPAREL, 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 INmune, our NK cell targeting platform.

Although INmune had interesting data in the treatment of hematologic diseases, we believe the future opportunities for INmune were greater by targeting and treating solid tumors. The CaRe PC trial using INmune to treat men with castrate resistant metastatic prostate cancers has made steady progress. We recently announced completion of dosing in the Phase 1 dose escalation part of the Phase I, Phase II trial and continue to dose patients in the Phase 2 part of the trial at the medium and high dose cohorts. As currently designed, we expect to complete dosing of patients with INmune 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 the new vial since 2018.

Dr. Mark Liddell 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 cords drumming kids with RDEB for the first time in November of 2024. The data our compelling and provides INmune Bio with a unique in-licensing opportunity that is INmune Bio owns and invented and owns cords from 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 own 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 or from 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 strong cell platform delivered intravenously, excuse me. 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 provides 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 courts from therapy on patients, quality of life seems clear. We believe this program is on a rapid path to the market where it will fulfil an unmet clinical need in kids with this desperately debilitating and ultimately lethal disease. While we love our cell therapy programs, we understand that ADO2 top-line data is the catalyst everyone, including ourselves are looking forward in the near term. At our core Immune Bio is a CNS company focused on Alzheimer’s disease. We have built this company around our XPro platform and analysis and a hundred days away from the results of the trial. In the Phase 2 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 make means. Our definition is simple, the data will provide unequivocal evidence of the impact of EXPAREL on the treatment and the clinical, and the response of those clinical symptoms of patients with early Alzheimer’s disease with biomarkers of information. This means we will provide a robust package of cognitive, clinical and functional data from patients treated with EXPAREL 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 EXPAREL 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 EXPAREL 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, EXPAREL 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 the slow the progressive decline.

We believe the results of this trial will challenge the longstanding plaques and tangle disease paradigm of Alzheimer’s disease, providing a fresh perspective on the treatment of the Alzheimer’s disease as an immunologic disease. We hope the first day of EXPAREL 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 ADO2, 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 physician’s 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 lymphoma aging becomes a reality. 2024 was a major, year of major accomplishments in all our programs. Great progress is 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.

David Moss : Thank you, RJ. As usual, I’ll provide a brief overview of 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 ADO2 data as defined in the warrant agreements, which if exercised or 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 a strong participation.

I cannot underscore have 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 million — $33.2 million for the year ended December 31st, 2024, compared with approximately $20.3 million for 2023. General and administrative expenses was 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 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 2 XPro trial for the treatment of neuroinflammation to cause Alzheimer’s disease in June.

We’re very excited that this key milestone for INmune Bio is now less than a hundred 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 2 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 ‘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 our debt sometime in the first quarter of next year. This is a seminal event for the company. If approved, it would be our first market therapeutic and transition us to 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 that 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: [Operator Instructions]. While we build that queue, we’ll take our first question from George Farmer with Scotiabank. Please go ahead.

Q&A Session

George Farmer: 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? And is there different requirements do you think for FDA approval and UK approval?

Raymond Tesi: Mark, you want to handle that?

Mark Lowdell: 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 we are 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 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 number of repeat treatments and the timing of those repeat treatments. And we will plan to do that trial both in the U.S. and in the UK.

George Farmer: Okay. Thanks. And then on EXPAREL, I think we’ve talked about how you intend to release the data in June. 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 results?

Raymond Tesi: CJ?

Christopher Barnum: Yes. 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. We will have all those clinical endpoints available.

George Farmer: In June…

Raymond Tesi : George, that means both, both EMACC and CDR will be released, when…

George Farmer: At the same time…

Raymond Tesi : When the data becomes public.

George Farmer: Okay. Thanks, RJ.

Operator: And we’ll next go to Paul Rader with BTIG. Please go ahead.

Thomas Shrader: Is that me, Paul Rader?

Raymond Tesi : I think that’s Tom Shrader.

David Moss : We knew who it was by the last name, go ahead Tom.

Thomas Shrader : I thought I’d been fired. Anyways. Good luck. It’s going to be the longest hundred days of your lives, but I don’t.

Raymond Tesi : It is.

Thomas Shrader : 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 to clarification, you said you’d screened 800, that was 800 after they were already neuro or inflamed, or is that 800 totals? And then one quick follow up on TR — if I ask 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

Raymond Tesi : CJ…

Christopher Barnum: Let me take the last one first. So, they are in 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 dysconnectivity 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 has always let us see the data. But what we’ve done is we’ve made sure that we’ve follow there, and I think we said this before, they have a playbook. We’ve followed it, and we think we’ve got as good a chance as I need 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 that 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.

Raymond Tesi : The screening — screen failure question.

Christopher Barnum: 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 a 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.

Raymond Tesi : If I can just add to if I can just add, reinforce what CJ said that next week is ADPD, which is the largest Alzheimer’s meeting in Europe, and we have a poster that was accepted that discusses the, shall we say, the profile of the patients that were enrolled. And you’ll see a presser on 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.

Mark Lowdell: And, 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 it’s and she highlights all of the key criteria and what we’ve done to meet them. It’s actually, worth your time.

Thomas Shrader: Great. Thank you.

Operator: Next, we’ll go to Gary Nachman with Raymond James. Please go ahead.

Denis Reznik: Good afternoon. This is Denis Reznik on for Gary Nachman. Thanks for taking the questions and congrats on all the progress. So first, on the EXPAREL Phase two 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 three 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.

Raymond Tesi: CJ, start with the dropout.

Christopher Barnum: Yes. 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 two 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 suggests we could power a study with 50 patients. The FDA may come back and say no, you need a larger safety database. We want a thousand 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, yes. 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’ll we’re going to move as fast as we can to get it going very quickly.

Dennis Reznik: 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?

Raymond Tesi: Go ahead, David.

David Moss: Yes. I’ll jump in. That’s a great question. And I think that’s actually probably also a prize with EXPAREL. 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 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, I mean, we’re working to get to a Phase 3 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’ll 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.

Denis Reznik: Thanks, so much.

Operator: Next, we’ll go to Elemer Piros with Rodman. Please go ahead.

Elemer Piros : 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?

Raymond Tesi : Mark?

Mark Lowdell : Yes, that’s true. We are in — the team in the UK manufactures and does all the process development and regulatory filing for both INmune and CORDStrom. And so now that INmune, all of the drug is made to complete the Phase 2 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 are 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.

Elemer Piros : Thank you. And maybe just a little follow-up there, but you are able to start the Open Label extension trial earlier then next year?

Mark Lowdell : Yes, as soon so the Open Label trial in the UK is ready to go. We already have the first dosage 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 parallel trial in the US, and that’s subjects to the funding environment which we live. But yes, we have an IND plan for the U.S. and the CTA is already approved in the UK.

Elemer Piros : Thank you, very much.

Operator: And our last question, our last question comes from James Molloy with Alliance Global Partners.

James Molloy : I had a question on the CORDStrom platform with the BLA coming in first quarter ‘26. Do you run up into any issues with the getting under the wire for the PRV program being granted, and any thoughts on what’s going on with the PRV that’s going to be renewed or not?

David Moss : Yes, Jim…

James Molloy : I’ll leave that to David.

David Moss : Yes, 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 going to — we’re working as quickly and diligent 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 U.S. 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 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 INmune submission, the INKBN 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.

Operator: I’d like to now turn the call back over to Dr. R.J. Tesi for closing remarks.

Raymond Tesi: So, we are busy. It’s heads down at INmune Bio as we get ever closer to our important readout in ADO2. 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 ADO2 goes and Alzheimer’s, the idea that inflammation, 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.

Operator: Thank you. And ladies and gentlemen, that does conclude today’s conference. We appreciate your participation, and you may disconnect at any time.