Greetings. And welcome to the INmune Bio First Quarter 2025 Earnings Call. At this time, all participants are in a listen-only mode. Later, you will have the opportunity to ask questions during the question-and-answer session. [Operator Instructions] 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 Dr., excuse me, Mr. David Moss, CFO of INmune Bio. David?

Thank you, Jessie, and good afternoon, everyone. We thank you for joining us for the call for INmune Bio’s first quarter 2025 financial results. With me on the call today are Dr. RJ Tesi, CEO of INmune Bio; and Dr. Mark Lowdell, Chief Scientific Officer of INmune Bio, who will provide an update on our CORDStrom and INKmune programs. Also on the call is Dr. CJ Barnum, Head of Neuroscience, who will be here to answer questions. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management in response to questions on this conference call are forward-looking statements under the Safe Harbors provisions of the Private Securities Litigation Form Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those such as forward-looking statements. Please see the forward-looking statements disclaimer on the company’s earnings press release, as well as risk factors in the company’s SEC filings, including our most recent quarterly filings with the SEC. There’s no assurance of any specific outcome. Undue reliance should not be placed on forward-looking statements which speak only as 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, now it’s my pleasure to turn the call over to RJ Tesi. RJ?

Thank you, David. For our first quarter 2025 call, I will review key takeaways and provide an update on our platform programs. Following my comments on recent developments, Dr. Mark Lowdell, INmune Bio CSO and inventor of both CORDstrom and INKmune, will provide an update on those programs. David Moss, INmune Bio CFO, will then conclude with a review of first quarter financial results and update future catalysts. Then we will be happy to take your questions. I’m sure everyone on this call knows we will soon be reporting topline results from MINDFuL, that is our Phase 2 trial in patients with early Alzheimer’s disease. The results are expected mid-to-late June. That is, in give or take 50 days, we will know the answer to the question, what happens in Alzheimer’s disease when you properly target neuroinflammation? Our last investor update call was just a short six weeks ago. But there have been important and I believe positive changes in the Alzheimer’s disease marketplace during that short period of time. We believe these changes will be beneficial to expose market opportunity in early Alzheimer’s disease. Last month at ADPD, which is the largest Alzheimer’s disease meeting in Europe, INmune Bio reported the biomarker profile of patients enrolled in the MINDFuL study. The data confirmed that we have been underestimating the market opportunity for XPro in patients with early AD. Historically, we stated that up to half of the early Alzheimer’s patients will qualify for XPro based on the biomarkers we used as our enrollment criteria. Based on the data INmune Bio and other companies presented at ADPD, we now believe more than two-thirds of early Alzheimer’s disease patients will be eligible for XPro based on ApoE4 status alone. I remind you that ApoE4 positivity was one of the four enrichment…

Thanks, RJ, and good afternoon, everyone, and thank you for joining us. So, with regard to the latest developments with INKmune, the CaRe PC trial in prostate cancer completed the Phase 1 dose escalation cohorts in December, which allowed us to open the Phase 2 extensions of both the high-dose and intermediate-dose cohorts in parallel, and we reported that in our last call. We saw no adverse events in any of the patients treated during Phase 1, which thus met the primary endpoint of the entire trial, and similarly, none of the patients treated in Phase 2 to-date has shown any adverse event, and INKmune remains extremely well-tolerated in this challenging and elderly group of patients who’ve had lots of previous treatment and a lot of comorbidities. At the end of March, we reported that INKmune infusions had led to increased NK cell potency in the patients treated at the lowest dose, and the blood samples from patients at the intermediate and high-dose cohorts of Phase 1 and Phase 2 are being received in the INmune Bio labs in London and are being prepared for testing. We’ll share those results as soon as they’re available. But in parallel, we’re receiving the independent reports of the PSMA PET screening of the Phase 1 patients who’ve completed follow-up. This is a very precise assay of the sizes of individual tumor lesions in each patient before treatment and at three months after completion of INKmune treatment. This very complex data set is being reviewed by the lead clinician for CaRe PC, but we can already see from subjects in the lowest dose cohort that some lesions have resolved completely following INKmune treatment. We eagerly await the data from the intermediate and high-dose patients, which we’ll share as soon as they become available. The…

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. Net loss attributable to common stockholders for the quarter ended March 31, 2025 was approximately $9.7 million, compared with approximately $11 million for the comparable period in 2024. Research and development expenses totaled approximately $7.6 million for the quarter ended March 2025, compared with approximately $8.7 million for the comparable period in 2024. General and administrative expenses were approximately $2.3 million for the quarter ended March 31, 2025, compared with approximately $2.3 million for the comparable period in 2024. At March 31, 2025, the company had cash and cash equivalents of approximately $19.3 million. Based on our current operating plan, we believe our cash is sufficient to fund our operations through Q3 of 2025. As of May 8, 2025, the company had approximately 23.2 million shares of common stock, outstanding. Subsequent to the end of the quarter, the company raised gross proceeds of approximately $2.1 million from the sale of common stock on the ATM. Now I’d like to focus on some key upcoming milestones. As everybody is well aware, we expect to have topline cognitive data from our Phase 2 trial on Alzheimer’s disease in the second half of June. As already stated, everyone at the company is looking forward to this event. We anticipate an end of Phase 2 meeting with the FDA in the fourth quarter of 2026 to agree on the design of a Phase 3 trial. We expect to complete enrollment in the Phase 2 portion of the INKmune trial this year, as Mark mentioned earlier, with periodic updates on immunologic and therapeutic responses to INKmune as data becomes available. We anticipate filing a BLA for CORDstrom in RDEB in the first half of 2026. Finally, we will initiate a Phase 2 trial of XPro in patients with treatment-resistant depression once NIH funding is made available. At this point, Jessie, I’d like to now poll for questions and open it up to Q&A. Jessie?

Thank you. [Operator Instructions] We’ll go first to Gary Nachman with Raymond James.

Hey, guys. This is Denis Reznik on for Gary Nachman. Thank you for taking our questions and congrats on all the progress. So, just assuming a positive readout in June, can you just continue walking us through the exact next steps for the program? You mentioned you can meet with the FDA at the end of this year, but what’s a realistic timeline as to when you can initiate the Phase 3? And then can you provide maybe some metrics as to what’s reasonable as to how many sites you can get online and how many patients could be enrolled each month? And then I’ve got a couple follow-ups.

Yeah. Well, this is RJ. So, thank you, Gary. But I think expecting us to really design the trial before we have the results and before we talk to the FDA, we would like to defer that opportunity. Our goal, as David mentioned in his milestones, is to, as quickly as possible, get to the FDA for an end of Phase 2 meeting. It is classified as a Type A/B meeting by the FDA process. So, there’s a 70-day clock. So, hopefully, as we said, it will be completed in the fourth quarter. And then we will move as quickly as possible to getting sites open and those first patients enrolled. We are lucky that we’ve got a lot of sites ready to go in Europe. So -- and we know there’s considerable enthusiasm for this program in the U.S. So, we anticipate being able to get the sites. But I don’t want to put a date on it. We don’t want to put a size on it. And because we can’t put a size on it, we don’t want to really predict what the capital needs will be at this point. But suffice it to say that, we believe that it will look very much like the Phase 2 trial, although we expect it will be larger and there may be a fewer set of biomarkers. But we won’t know until we talk to the FDA.

Totally understand that. And that’s helpful color. Just a couple quick follow-ups. Just because there’s been a lot of turnover and uncertainty at the FDA recently, can you comment on if the people who will be reviewing your program are also there? Everyone who’s previously signed off on the EMAC is also there? And then with the post-presentation you guys had at ADPD last month, maybe can you just talk a little bit more about the receptivity you’ve received at the conference and then overall the level of interest the company has been receiving recently as we approach its June readouts?

Yeah. I’ll let CJ answer the ADPD call. But we’ve obviously, like any biotech, have been watching what’s going on at the FDA quite closely. We -- our intelligence, which is pretty good, we believe, suggests that when it comes to drug development, the FDA has remained on track. Delays appear to not be developing that everyone feared. We can’t predict the future, but everything we hear so far is okay. I remind you that the FDA has not yet completely signed off on EMAC. Our goal is -- and CJ can add more color to this, our goal is to present them EMAC data side-by-side with the CDR data. And one of the major questions we’ll be asking them at the end of Phase 2 meeting is, can we use EMAC as the primary endpoint for the registration trial? Remember, and we’ve been saying this forever, that we believe that it’s our superior metric of cognitive function in these patients. But it’s the FDA’s sandbox. And if they say, no, we’re not happy, but we will move ahead with CDR. And in fact, the trial that we are currently doing will allow us to perfectly design the study to get the kind of result we need. CJ, you want to add any color to that and also comment on his ADPD question.

Yeah. Yeah. Sure. Just to sort of give you, clarify a little bit about what we’ve communicated with the FDA is we’ve given them the plans and what we intend to do with EMAC. And what they’ve done is they’ve responded to that in a way that really says that outlines their guidelines on how you validate a measure, really thinking about it more like a checklist, which is what we’ve done in this trial. So, they’re not going to comment on that until they see the data. That’s just a standard response. But we think we’ve done everything. We’ve hit all those bullets in those checklists and I think we’re in a good position. ADPD was pretty interesting. I think there’s two things that I think really came out of it as it relates to feedback we got from the poster. One is I think people are excited for an anti-amyloid or a therapy that’s not targeting anti-amyloid. And I would say even more so, we’ve got a lot of traffic and interest in EMAC. And one of the comments that we, especially from neuropsychs that work with big companies or work in the space and measuring cognition, are really excited that there’s a company that’s driving the appropriate measures moving forward. So, there’s a lot of excitement and interest around the outcome there.

Great. Thanks so much. We’re looking forward to the readout.

We’ll move next to George Farmer with Scotiabank.

Hi. Good afternoon. Thanks for taking my questions. A couple for me on XPro. So, with the trial coming up and the data coming up, what -- how do you think investors will react to a scenario whereby you hit on EMAC but CDR is a bit equivocal? And then, RJ, you were talking about the potential benefit of XPro in patients who would be ineligible for anti-amyloid therapy, including ApoE homozygous. Do you have a feel for how many ApoE homozygous are in your trial?

Yeah. So, CJ, why don’t you address the specific question about hitting on EMAC and what CDR will look like? Because it will be more correlative than not.

So, yeah, I’m not sure where you’re going with that, RJ. But let me just, to answer the question about, how investors feel, I actually would ask you that question. From a scientific standpoint, what I can tell you is that the EMAC is the tool that’s actually capturing cognitive changes that occur in early AD. It’s identifying those patients. It’s the ability to measure cognitive decline. It’s the right tool. The CDR is a more blunt instrument. I think RJ -- I think what RJ is saying is, one of the things that we’re seeing is it correlates very well. So we’re seeing correlations between EMAC and CDR, which is a good sign. But the CDR is inherently more noisy because it’s a blunt tool. So I would say, well, I can’t answer how the investors would think. And I’m hopeful that we’ve talked with enough of you so that you understand how we think in the scientific validity and rationale for using the EMAC. For us, the EMAC is really the primary driver and we’ll understand what if the EMAC, for example, is fuzzy. We’ll have a clear understanding. The most likely scenario is just it’s a power issue due to noise. But we won’t know until we see the data.

Yeah. And just to add a little bit more color, we believe that professionals in the field, i.e., the academics and potential biopharma partners, will be able to understand if there is -- they don’t both, aren’t both perfect. And as CJ says, it’s not going to be that CDR is going in a different direction. It’s just going to be a power and a size of study issue, which is easily solved in the Phase 3 trial. Yeah, so let’s talk about the ApoE4 homozygotes. In both the lecanemab and the donanemab trial, they were 15% of the patients. In our trial, it is 9%. They’re smaller trials. I don’t see 15% and 9% that difference. So I expect it will be in the 15% range. Interesting, aducanumab did not break out the homozygotes in number. At least I don’t remember it. So I think it’s a pretty, and when you go into the literature and you look at clinical data, that’s about where it stands. So that’s a pretty, in Europe, it’s a big population. And as you know, in Europe and the U.K., they don’t do off-label prescribing. So that group is ready and waiting for XPro, in my opinion.

All right. Great. And then one more from me. The impact of XPro on Phospho-tau 217 looks pretty compelling. Went back and looked at your presentation. How do you think that magnitude compares to other Alzheimer’s disease treatment approaches that have been published?

CJ, I’m going to leave that one to you.

I think that’s tough to answer. I think the only thing that I can say is you don’t rarely, I can’t think of another study where you saw changes in the CSF that early quite robustly. I think this is one of those things that holds a lot of promise. But we’ll see what it looks like when we have the full data set.

Yeah. We’re the only company with data in a drug that treats neuroinflammation. The anti-amyloid drugs do decrease tau. I mean, I think when neurons stop dying, you see -- you get some decrease in tau. But we like p-tau217. The clinical teams like p-tau217. And I suspect most of the regulatory agencies are going to be very receptive to that biomarker as part of our data package.

Okay. Thanks very much.

Thank you.

We’ll go next to Tom Shrader with BTIG.

Good afternoon. Thanks for taking the questions. You said something that I hadn’t really thought of, and I’m wondering if it’s correct, if it’s -- if I’m hearing, but are ApoE4 patients inherently inflammatory? And then the other question, I kind of want to re-ask George’s question with a little bit of a, how much does CDR have to decline? How big does the reduction in decline of CDR have to be to hit in a trial of 300 patients that’s only run for six months? Is it reasonable or is it a pipe dream? Do you have a sense of what the reduction in decline would have to be for a trial of this size to hit? Thanks.

Okay. Yeah. I can take that. I can take the first one…

CJ?

… or the second one. So, Tom, what’s interesting is, when we powered the study, which was powered on CDR, by the way, the assumptions that we had in terms of our expectation for decline over six months, and the effect size of that decline was somewhat conservative based on the ADME group that was used to power the study. What’s interesting is, a few years later, when lecanemab and donanemab came out, what we saw was the assumptions that we used were exactly what happened. So, within a six-month period, both aducanumab or lecanemab and donanemab were statistically significant at six months. And their decline was about the exact same number that we used to decline for six months. And I think that’s important. And the effect size of that decline was almost exactly what we used to calculate our power. So, I think that gives us a lot of confidence that, our assumptions were right on. I think the other thing that I want to point out is, is this for a cohort of patients that weren’t enriched for inflammation. And of course, we expect that we’re going to get a little bit faster decline with inflammation. So, I think that gives us even a little more confidence.

Can I?

Yeah. And ApoE4 is considered an inflammation gene. It is considered that with your ApoE4, you are hot, so to speak. And as CJ just said, if you look at ApoE4, either heterozygotes or homozygotes, they actually get, they -- their age of onset is earlier, with the heteros being later than the homozygotes. Their progression of the disease, i.e., going from MCI to early mild AD is faster. And actually, when you look at the ApoE homozygotes, ApoE4 homozygotes, they actually have a higher mortality rate. They have about a five-year to seven-year worse survival compared to the other groups. So, ApoE4 is a bad gene to have. And any of you that have done 23andMe and they ask that question, do you want to know what your Alzheimer’s risk is? The main thing they’re going to tell you was there -- was whether or not you were ApoE4 positive. And I don’t know how many said yes, but I never wanted to know, quite frankly, so.

If I can follow up with, with CJ, how much of the other two trials hitting, they’re bigger trials, right? There’s something like, I don’t know, there’s a few fold more patients. Is that the reason they separated in six months, or do you still think you’re powered correctly to see it if you have a similar type effect?

Well, I think, so -- I mean, there’s some variables we don’t know. I think we’re close. I don’t think we’re going to be off too much. So, it’s hard to answer that question, but I would say that, the data that we see, despite the fact that they’ve got more patients, we’re looking at standard deviation. The standard deviation was around 1 for those, for those trials, which is, which is very similar to what we used in our projections and the decline was quite similar. So, I think we’re going to be okay. I think we’re going to be close.

And Tom, remember we…

We bragged about the quality control that we’ve had in this trial.

Yeah.

The procedure of the type of patient we enrolled. I think that is really an unheralded advantage. When you’re enrolling 1,600 patients, and I think it was like in 42 countries or something as those big trials, the quality control -- you just get a messier patient population. It’s not because people aren’t trying. It’s just it’s a big animal pain. And I can tell you, we’ve spent a huge amount of time and resources on our quality control, and our trial was much smaller. It was, what, 208 patients in eight or nine countries. So, the quality in will be reflected in the output, I believe.

All right. Great. Thanks for all the color.

Our final question will come from James Molloy with Alliance Global Partners.

Hello. This is Laura Suriel on for Jim Molloy. Thank you for taking the questions. So, for CORDstrom, are you still on track to initiate the 12-month open-label trial with this year? And I also see that U.S. patients are expected to be enrolled later on. So, what’s the enrollment aim here, and how many sites do you expect to have open in the U.S.?

Mark?

Yeah. Great. Thanks very much for that question. What we’re doing at the moment is following the guidance from the FDA about how to make the U.K.-manufactured cords usable in the U.S., and we’re starting a manufacturing program later this week, actually, of a new batch of products using U.S.-approved cord donors. So, that allows us, once we have those data, to draft the IND. We’re expecting to submit an IND later this year. We’ve been delayed by various factors, including the funding situation. But we’re still on track to or still planning an IND in the U.S. for CORDstrom. But it’s not -- the BLA is not dependent upon the U.S. IND, or indeed, the open-label in the U.K. We’re going to submit for the BLA with the data we already have from the double-blind placebo-controlled crossover trial, and then we will run a follow-on trial in the U.S. opening next year, in parallel with trials in the U.K., in which we will further explore the dosing of the drug and the periodicity of dosing. Does that answer your question?

Yes. It does. Thank you. And Just as a follow-up, with the BLA finally coming up, how would you describe the overall regulatory space for RDEB treatments? Like, Abeona, for instance, just got approval for their gene therapy for RDEB. So, do you consider this a positive…

Yeah.

… for where you’re at with CORDstrom?

There are two things about that. That’s a very good question. So, the synthetic skin gene-modified product, which has just been licensed, it’s a great product. The challenge is that it’s applicable to open wounds on the skin and that’s its only indication, and it requires a surgical intervention to apply it. One of the known side effects is itch, and obviously, one of our principal clinical outcomes from the first trial has been reduction in itch. So, even in the presence of the gene-modified product, we have a window to treat the same patients with CORDstrom. But more importantly, CORDstrom is a systemic therapy, and as I said in the presentation just a few minutes ago, RDEB, and indeed all EB, is actually a systemic disease, and these kids, and indeed when they get through to adulthood, they suffer the condition throughout their esophageal tract, and they’re more widespread than just the dermis. And so, we see a role for CORDstrom in treating those patients with systemic disease, as well as skin lesions. Indeed, a trial of a similar MSC product that’s not going through to license in South Korea showed improvement in skin scores after treatment as well, when the children were followed up long enough. So, we do see a really good opportunity for CORDstrom, even in the presence of the current licensed alternatives.

Understood. Thank you for taking the questions.

And now that will conclude the Q&A portion. I will turn the program back over to Dr. Tesi for any additional or closing remarks.

Yes. Thank you all for attending today’s call and I will just make a moment of closing comments, because we are excited. We are approaching the most significant milestone in the company’s history. When we started INmune Bio and got XPro in 2017 and became a company focused on Alzheimer’s disease, no one viewed it as an immunologic disease, or few did. At that time, the focus was exclusively on amyloid and tau. Since then, with two anti-amyloid drugs on the market, we have seen a key change in the way Alzheimer’s disease is viewed. Alzheimer’s is considered by many a CNS disease driven by immune dysfunction. Neuroinflammation is no longer viewed as a side effect of Alzheimer’s disease pathology, but a significant driver of that pathology. INmune Bio has positioned itself as a leader in targeting the immune dysfunction that drives destructive neuroinflammation. We are very careful and precise with our terminology here. Stopping neuroinflammation by immunosuppression, glial suppression, is very different than stopping destructive neuroinflammation by repolarizing glial cells to support the CNS cellular unit and improving remodeling and repair. The goal of effective therapy for Alzheimer’s disease is to reestablish normal glial homeostasis. The idea that the brains of the elderly with dementia can undergo remodeling and repair is novel. We believe data from the MINDFuL trial will change the direction of scientific research and discovery in the neurology and CNS drug development arena. I’ve said before that this is the dawn of the golden age of CNS development. We believe it is and we look forward to leading the charge. So, with that, I thank you, and I am -- we will be talking to you all soon when the data are released. So, thank you very much.

Thank you. Ladies and gentlemen, this does conclude today’s program. Thank you for your participation. You may disconnect at any time.