INmune Bio Q1 2025 Earnings Call Transcript

Quartr
Provided by Quartr
May 8, 2025

There are 9 speakers on the call.

Operator

Greetings, and welcome to the Immune Bio First Quarter twenty twenty five 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. As a reminder, this conference is being recorded. A transcript will follow within twenty four hours of this conference call.

Operator

At this time, it is my pleasure to introduce Mr. David Ma, CFO of Immune Bio. David?

Speaker 1

Thank you, Jesse, and good afternoon, everyone. We thank you for joining us for the call for Immune Bio's first quarter twenty twenty five financial results. With me on the call today are Doctor. RJ Tesi, CEO of Immune Bio and Doctor. Mark Lodell, Chief Scientific Officer of Immune Bio, who will provide an update on our cord strumming immune programs.

Speaker 1

Also on the call is Doctor. 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 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 filings with the SEC.

Speaker 1

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, Immu 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 Tessi. RJ?

Speaker 2

Thank you, David. For our first quarter twenty twenty five call, I will review key takeaways and provide an update on our platform programs. Following my comments on recent developments, doctor Mark Liddell, immune bio CSO and inventor of both Korchtram and Inkmune, will provide an update on those programs. David Moss, immune bio's 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.

Speaker 2

I'm sure everyone on this call knows we will soon be reporting top line results from MINDFUL. That is our phase two trial in patients with early Alzheimer's disease. The results are expected mid to late June. That is in give or take fifty 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 AD market Alzheimer's disease marketplace during that short period of time.

Speaker 2

We believe these changes will be beneficial to Xpro's market opportunity in early Alzheimer's disease. Last month at ADPD, which is the largest Alzheimer's disease meeting in E in The in Europe, Immune Bio reported the biomarker profile of patients enrolled in the MINDBLE study. The data confirmed that we have been underestimating the market opportunity for EXPAREL in patients with early AD. Historically, we stated that up to half of the early Alzheimer's patients will qualify for EXPAREL based on the biomarkers we used as our enrollment criteria. Based on the data in new 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 APOE four status alone.

Speaker 2

I remind you that APOE four positivity was one of the four enrichments or enrollment criteria we used in the MINDFUL study. The APOE four status of patients in the MINDPLES is almost identical to what is reported in recent major trials in Alzheimer's. Patients with at least one APOE four allele make up more than two thirds of the patients in these trials. This means the market opportunity for EXPAREL in early AD has increased to nearly seventy percent of early AD patients, not the forty percent we have previously been talking about. On the call six weeks ago, I also mentioned the safety profile of EXPAREL in mindful trial.

Speaker 2

Nothing has changed. There are no reports of area. No patients have had unscheduled MRIs due to CNS symptoms or, you know, headache, etcetera, and there have been no deaths. So far, EXPAREL is safe and well tolerated in this patient population that has an average age of 73 years old, and many of them have a long list of comorbidities. The excellent safety profile of EXPAREL in these patients provides a unique APOE four related market opportunity for EXPAREL.

Speaker 2

Let me explain. Both The EU and The UK have approved mecanumab, the acai biocin drug, for patients with early Alzheimer's disease who have none or one copy of the APOE four gene. The market authorizations specifically exclude patients who carry two APOE four alleles. In the early AD trials that report APOE four status, APOE four homozygotes, that's the patients that have two APOE four alleles, are fifteen percent of the patients. That means because of labeling restrictions on mecanumab in The UK and EU, Early APO early Alzheimer's patients who are APOE four homozygotes will not be eligible for therapy with the anti amyloid drugs.

Speaker 2

This group now is an important unmet need ideally suited for EXPAREL therapy. In The US, recent surveys of practice patterns indicate that this patient population is not treated in many centers due to risk variance. So even in The US where the labeling is different than you see in The UK and Europe, we believe that after approval, EXPAREL will be the best and only treatment option available for this subgroup, important subgroup of early Alzheimer's patients. We should have an exclusive biologically based market. Finally, the biomarker landscape of Alzheimer's disease is really evolving quite quickly, and it's evolving in a way that highly that really benefits our focus in these patients.

Speaker 2

Now once the diagnosis of Alzheimer's is made, p tau two seventeen in blood has become the biomarker of most important interest by clinical teams treating these early Alzheimer's patients. P tau two seventeen levels define the severity of Alzheimer's. P tau two seventeen levels in the blood have prognostic value and correlate with stage of disease. In the near future, we predict the changes in p tau two seventeen blood levels will be used as a pharmacodynamic blood marker of therapeutic response in these patients. As a reminder, Xpro significantly decreased p tau two seventeen during the three month phase one study, and this biomarker is included in the package of biomarkers that we are studying as in the mindful phase two program.

Speaker 2

Having a great drug is net is a necessary element for a successful clinical program, but it is only part of the story. Since the last patient was enrolled in November, we have been highlighting the hard work needed to report the top line data in June. These are the busiest of times. For example, after the last patient has their final safety visit, but before the database is locked, a complex series of critical data management and quality assurance tasks are undertaken to ensure the data are complete, accurate, and ready for analysis. The process begins with data cleaning where we review case report forms and entries into the electronic data capture system and to resolve discrepancies, fill in missing data, and look for outliers.

Speaker 2

This is a patient by patient process. It is labor intensive. Queries are issued to trial sites to clarify inconsistencies, and there is source data verification to confirm that the recorded data matches the source documents, for instance, the medical records. This phase also involves ensuring compliance with regulars regulatory standards such as GCP as to by maintaining lot trails and documenting all changes. After data cleaning are complete, the focus shifts shifts to the final quality checks and preparation for database lock.

Speaker 2

A comprehensive review of the data is performed to confirm that all queries are resolved, deviation is documented, and validation checks satisfied. The statistical plan cross check to ensure that all data points are present and correctly formatted, and the data monitoring committees conduct final safety and efficacy reviews. We don't lock the database until we are sure the database is clean and accurate. I will also say that this is all done with blinded data. No one knows who got what during this process.

Speaker 2

We don't run the statistical programs until the database are locked. And it's only when that statistical package comes out that the real unblinding occurs. We remain on track for this process to be completed in mid to late June, and I can tell you we can hardly wait to see the fruits of our labors. This is the moment we've been anticipating for several years. We are confident we will report results that will change the care of patients with early Alzheimer's disease, and this confidence is highlighted by man management's substantial show share ownership.

Speaker 2

Like you, we are investors in immune bio. Our interests are aligned with yours. As important as mindful our Alzheimer's trial is to the company and our investors, it's not our only program. Corridstrom for the treatment of children with recessive dystrophic epidermolysis bullosis or RDEB is expected to file a BLA in 2026. The Inkmune program continues to move forward in men with metastatic castrate resistant prostate cancer.

Speaker 2

The light is shining more on more brightly on courts from these days. It is an orphan disease program. And after recent comments from the FDA, we are increasingly excited by its prospects. The FDA has stated their intention to move rare disease treatments through the approval process faster with more input from patients and caregivers. In our gov, Nordstrom provides a systemic therapy for systemic genetic disease that has the support of patients and caregivers.

Speaker 2

But enough from me. I will turn this over the microphone over to Mark Liddell, our CSO and inventor of both courtship and Inkmune to give you a more in-depth update on those programs. Mark? Thanks,

Speaker 3

RJ, and good afternoon, everyone, and thank you for joining us. So with regard to the latest developments with INCMEON, the CAREPC trial in prostate cancer completed the phase one dose escalation cohorts in December, which allowed us to open the phase two 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 one, which thus met the primary endpoint of the entire trial. And similarly, none of the patients treated in phase two 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 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 one and phase two are being received in the immune bio labs in London and are being prepared for testing.

Speaker 3

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 one 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 inkling treatment. This very complex data set is being reviewed by the lead clinician for CarePC, but we can already see from the subjects in the lowest dose cohort that some lesions have resolved completely following the immune treatment. We eagerly await the data from the intermediate and high dose patients, which we'll share as soon as they become available.

Speaker 3

The CARE PC trial continues to recruit phase two subjects and remains on track to complete enrollment this year. The immune bio team has manufactured all doses of INKVIEN for the completion of the trial, and we've successfully transitioned The US drug supply logistics from our previous contractor into a US company called Cryoport, so we're set up for the successful conclusion of the trial. In line with our ambitions for INKVIEN in prostate cancer and other solid tumors, we're transitioning our manufacturing into a UK government incubator facility where we can manufacture future drug batteries for clinical trial and if successful, commercial manufacture and global supply. But while CAREPC is ongoing, in February, as IJJ has said, we announced the development of our Cordstrom asset towards a BLA filing next year twenty twenty six for the treatment of the extremely debilitating disease recessive dystrophic epidermolysis bullosa or RDEB. Eptomolysis bullosa, of which RDEB is the most severe form, is an inherited disease which manifests in the first two years of life.

Speaker 3

The outer layer of the skin, the epidermis, doesn't anchor properly to the underlying dermis, and children suffer horrific skin blisters over their whole body. Worse still is that EB is a systemic disease, as RJ said. So children suffer with lesions behind their eyes, down their esophagus, and throughout their gastrointestinal tract. There's no systemic treatment for RDEP. Cordstrom is an off the shelf allogeneic mesenchymal stromal cell drug from pooled donors, which Immune Bio has owned since 2019.

Speaker 3

It was developed by me and some colleagues with academic funding in The UK and is a platform that can be used to treat multiple clinical indications by specific selection of the individual donor products used to formulate the final pooled drug. We've been selling one formulation of Cortstrom into The UK multicenter trial led by pediatricians from Great Ormond Street Children's Hospital in London to treat children with with RDEB. This was a double blind, placebo controlled crossover trial, which treated all of the eligible children in The in England with RDEB. The results when they were unblinded led to the clinicians and the UK National Institute of Health Research asking immune bio to develop cordstrom as a licensed medicine for this disease, and we presented the trial data to The US FDA in December as RJ said. The FDA data review led to the award of rare pediatric disease and orphan drug status for the treatment of epimole epidermoid spilosa.

Speaker 3

And following a type c meeting with the FDA in February, we have a clear route to submission of a BLA in 2026 and parallel submissions to the UK MHRA and to the European Medicines Agency. On our last call, we said that clinical trials are the poster children of drug development, but moving from trials to market requires much more, not least a full development of the drug manufacturing pathway, which meets regulatory requirements, is cost effective at scale, and meets likely global demand. We've taken this on board with respect to Ichordstrom in the same way we have with INKVIEW and, in fact, have developed parallel processes for both drugs, which can share the same manufacturing platforms at all stages of manufacture. This not only simplifies manufacturing facility setup and design, but it allows us to maximize the use of manufacturing space we rent by being able to switch between inkling production and cordstrom manufacture, thus controlling our production costs as we move towards commercial supply. Having used the income from selling cordstrom into The UK trial in EB to subsidize the supply of Inkmune into CarePC, the equipment we've been using to manufacture Inkmune is now subsidizing the development of Kordstrom, which is a nice, very circular situation.

Speaker 3

Having completed all manufacture of Inkmune for CarePC, the UK team is dedicated to providing all of the data needed for the BLA submission next year for Cordstrom and transitioning into the new production space to allow Cordstrom as a commercial product and Inkmune as an investigational product for our next clinical trials. So that ends my update on the Inkmune and Cordstrom platforms. Just to say we're as excited about these as we are about the AD-two trial. And I'd like to turn the call over to David Moss, our CFO, discuss financials. David?

Speaker 1

Thank you, Mark. As usual, I'll provide a brief overview of our financial results and upcoming milestones before we head to our Q and A session. Net loss attributable to common stockholders for the quarter ended 03/31/2025 was approximately $9,700,000 compared with approximately $11,000,000 for the comparable period in 2024. Research and development expenses totaled approximately $7,600,000 for the quarter ended March 2025 compared with approximately $8,700,000 for the comparable period in 2024. General and administrative expenses were approximately $2,300,000 for the quarter ended 03/31/2025, compared with approximately $2,300,000 for the comparable period in 2024.

Speaker 1

At 03/31/2025, the company had cash and cash equivalents of approximately $19,300,000 Based on our current operating plan, we believe our cash is sufficient to fund our operations through Q3 of twenty twenty five. As of May 2025, the company had approximately 23,200,000.0 shares of common stock outstanding. Subsequent to the end of the quarter, the company raised gross proceeds of approximately $2,100,000 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 top line cognitive data from our phase two trial in Alzheimer's disease in the June.

Speaker 1

As RJ stated, everyone at the company is looking forward to this event. We anticipate an end of Phase two meeting with the FDA in the fourth quarter of twenty twenty six to agree on the design of a Phase three trial. We expect to complete enrollment in the phase two portion of the INCMEUN trial this year as Mark mentioned earlier, with periodic updates on immunologic and therapeutic responses to INCMEUN as data becomes available. We anticipate filing a BLA for Kordstrom in RDB in the first half of twenty twenty six. Finally, we will initiate a phase two trial of EXPAREL in patients with treatment resistant depression once n I NIH funding is made available.

Speaker 1

At this point, Jesse, I'd like to now poll for questions and open it up to Q and A. Jesse?

Speaker 3

Thank you.

Operator

We'll go first to Gary Nachman with Raymond James.

Speaker 4

Hey, guys. This is Dennis Resnick 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.

Speaker 4

But what's a realistic timeline as to when you can initiate the phase three? And then could 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 of follow ups.

Speaker 2

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 is we would like to defer that opportunity. Our goal, as as David mentioned in his milestones, is to, as quickly as possible, get to to the FDA for a end of phase two meeting.

Speaker 2

It is classified as a type a b meeting by the FDA, you know, process. So there's a a 70 do 70 clock. So, hopefully, as 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 US.

Speaker 2

So we anticipate, you know, being able to get the sites, but I don't wanna put a date on it. We don't wanna put a size on it. And because we can't put a on it, we don't wanna really predict what the capital needs will be at this point. But suffice it to say that, you know, we believe that it will look very much like the phase two trial, although we expect it will be larger. And, you know, there may be a a fewer set of biomarkers, but we won't know until we talk to the FDA.

Speaker 4

Totally understand that, and that's helpful color. Just a couple quick follow ups. Just because there's been a lot of turnover and certainty at the FDA recently, can you comment on if the people who will be reviewing your program are all still there? Everyone who's previously signed off on the EMAC is all still 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 received at the conference and then overall the level of interest the company has been receiving recently as we approach June readouts?

Speaker 2

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. The delays appear to not be, you know, be developing that everyone feared.

Speaker 2

I you know, 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 two meeting is, can we use EMAC as the primary endpoint for the registration trial? Remember, and we've been saying this forever that, you know, we believe that it's our superior metric of cognitive function in these patients.

Speaker 2

But it's the FDA sandbox. And if they say no, we we'll move we're hap we're not happy, but we will move ahead with CDR. And in fact, you know, the trial that we are currently doing will allow us to perfectly design the study to get the kind of result we need. DJ, you wanna add any color to that and also comment on his ADPD question? Yeah.

Speaker 5

Sure. Just to sort of give you clarify a little bit about what what we've communicated with the FDA is we've we've given them the plans and what we intend to do with with the EMAC. And what they've done is they've responded to that in a way, that really says that outlines their guidelines on on how you, validate a measure. Really, think about it more like a checklist, which is what we've done in this trial. So, you know, they're not gonna comment on on that until they see the data.

Speaker 5

That's just a standard response. But we think we've done everything. We've we've hit all those bullets in those checklists, and I think we're in a good position. ADP was pretty interesting. I think there's there's two two things that I think really came out of it as it relates to feedback we got from the poster.

Speaker 5

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 we got a lot of traffic and interest in EMAC. And, and one of the comments that we especially from neuropsychs that work with big companies or worked in the space in in measuring cognition are really excited that there is a company that's driving the appropriate measures moving forward. So there's a lot of excitement and interest around the outcome there.

Speaker 4

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

Operator

We'll move next to George Farmer with Scotiabank.

Speaker 6

Hi. Good afternoon. Thanks for taking my questions. A couple from me on Xpro. So with 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.

Speaker 6

And then, you know, RJ, you were talking about the potential benefit of Xpro in 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?

Speaker 2

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,

Speaker 5

yeah, I'm not I'm not I'm not sure where where you're going with that, RJ. But let me just you know, to answer the question about, you know, how investors feel. I I actually would ask you that question. You know, from a scientific standpoint, what I can tell you is is that the EMAC is is the tool that's actually capturing cognitive changes that occur in early AD. It's it's it's identifying those patients.

Speaker 5

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.

Speaker 5

But the the CDR is inherently more nose noisy because it's, because it's a blunt tool. So I would say well, I can't answer how the investors would think, and I'm I'm hopeful that we've we've talked to with enough of you so that you understand how we think in the scientific validity, and rationale for using the EMAC. For us, the 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 it's a it's a power issue due to noise.

Speaker 5

But we won't know until we see the data.

Speaker 2

Yeah. And 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 you know, they don't both aren't both perfect. And as CJ says, it's not gonna be that CDR is going in a different direction. It's just gonna be a a power and a size of study issue, which is easily solved in the phase three trial. Yeah.

Speaker 2

So let's talk about the APO p e four homozygotes. In both the lucanumab and the donanemab trial, they were fifteen percent of the patients. In our trial, it is nine percent. They're smaller trials. I don't see fifteen and nine percent that difference.

Speaker 2

I expect, you know, it will it will be in the fifteen Interesting. Aducanumab does did not break out the homozygotes in number. At least I don't remember it. So I think it's a it's a pretty and when you go into the literature and you look at clinical data, that's about where it stands.

Speaker 2

So that's a pretty you know, in Europe, it's a big population. And as you know, in Europe and The UK, they don't do off label prescribing. So that group is ready and waiting for in my opinion.

Speaker 6

Mhmm. Alright. Great. And then one one more for me. You know, the impact of Xpro on on phospho tau two seventeen looks pretty compelling.

Speaker 6

Went back and looked at your presentation. How did how do you think that magnitude compares to other Alzheimer's disease treatment approaches that have been published?

Speaker 2

DJ, I'm gonna leave that one to you.

Speaker 5

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

Speaker 2

Yeah. We're the only we're the only company with data in a drug that treats neuroinflammation. You know, the anti amyloid drugs do decrease tau. I mean, I think when you when when neurons stop dying, you see know, you get some decrease in tau. But we like p tau two seventeen.

Speaker 2

The clinical teams like p tau two seventeen, and I suspect most of the regulatory agencies are gonna be very receptive to that biomarker as part of our data package.

Speaker 6

Okay. Thanks very much. Thank you.

Operator

We'll go next to Tom Schrader with BTIG.

Speaker 7

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 if I'm hearing, but are APOE four patients inherently inflammatory? And then the the another question, I I kinda wanna reask George's question with a little bit of a how 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?

Speaker 7

Is it is it reasonable, or is it is is it a pipe dream? Do do you have a sense of what the reduction in decline would have to be for a trial of this side size to hit? Thanks.

Speaker 5

Okay. Yeah. I can take that. Can take the first one. Steve, pardon the second one.

Speaker 5

So so, Tom, what's interesting is when we, when we powered the study, which which was powered on CDR, by the way, the assumptions that we had in terms of our expectation for decline, over six months and, and the effect size of that decline, was somewhat conservative based on the ADNI group that was used to power the study. What's interesting is, you know, a few years later when lucanumab and and dananemab came out, what we saw was, the assumptions that we used were exactly what happened. So within a six month period, both, aducanumab or lucanumab and dananemab were statistically significant at six months. And their decline is 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.

Speaker 5

So I think that gives us a lot of, a lot of confidence that, you know, our assumptions were were right on. Think the other thing that I wanna point out is is this is for a cohort of patients that weren't enriched for inflammation. And, of course, we expect that we're gonna get a little bit faster decline with inflammation. So I think that gives us even a little more confidence.

Speaker 2

Can I tell you what's the would be considered an inflammation gene? It is considered that with your APOE four porous, you are you are hot, so to speak. And as as CJ just said, if you look at APOE four either heterozygotes or homozygotes, they actually get they they their age of onset is earlier with the heterose being later than the homozygotes. Their progression of the disease, I. E, going from MCI to early mild AD is faster.

Speaker 2

And, actually, when you look at the APOE homozygotes, APOE four homozygotes, they actually have a higher mortality rate. They have about a five to seven year worse survival compared to the other groups. So APOE four is a is is a bad gene to have. And any of you that have done 23 and me, you know, and they they ask that question, do you wanna know what your Alzheimer's risk is? The main thing they're gonna tell you was there was whether or not you were APOE four positive.

Speaker 2

And I don't know how many said yes, but I never wanted to know quite frankly.

Speaker 7

So If I I can follow-up with with CJ. How much of the other two trials hitting they're bigger trials. Right? They're something like, you know, 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 you're powered correctly to to see it if you have a similar type effect?

Speaker 5

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

Speaker 5

And and the decline was was was was quite similar. So I think I think we're gonna be okay. I think we're gonna be close.

Speaker 2

And, Tom, remember, we have bragged about the 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 an unheralded advantage. You know, 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 populations, not because people aren't trying.

Speaker 2

It's just it's a big animal to pain. You know? 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 the quality in will be reflected in the in the output, I believe.

Speaker 7

Alright. Great. Thanks for all the color.

Operator

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

Speaker 8

Hello. This is Laura Suriel on for Jim Malloy. Thank you for taking the questions. So for Cordstrom, are you still on track to initiate the twelve month open label trial mid this year? And I also see that US patients are expected to be enrolled later on.

Speaker 8

So what's the enrollment aim here, and how many sites do you expect to have open in The US?

Speaker 5

Mark?

Speaker 3

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 UK manufactured, cords, usable in The US, and we're starting the manufacturing program later this week, actually, of a new batch of products using a US approved cord donors. So that allows us once we have those data to draft the IND.

Speaker 3

We're expecting to submit, an IND late this year. We've been delayed by, various factors including the the, the funding situation. But we're still on track to to also planning, an IND in The US for cordstrom, but it it's not the BLA is not dependent upon the The US IND, or indeed the the open label in The UK. We're going to submit for the BLA with the data we already have from the double blind placebo controlled cross crossover trial, and then we will run, a follow on trial in The US, opening next year in parallel with trials in in The UK in which we will further explore, the dosing of of of the drug and the periodicity of, of dosing. Does that answer your question?

Speaker 8

Yes. It does. Thank you. And, just as a follow-up, with the BLA filing coming up, how would you describe, like, the overall regulatory space for RDEB treatments? Like, Abeona, for instance, just got approval for their gene therapy for RDEB.

Speaker 8

So do you consider this a positive for where you're at with Cordstrom?

Speaker 3

So there are two things about that. That's a very good question. So the the, synthetic skin, gene modified product, which has just been licensed, but it's a great product. The challenge is that it's it's applicable to open wounds on the on the, skin, and that's its only indication. And it requires a surgical intervention to to apply it.

Speaker 3

One of the side effects is 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 of the Gene Modified product, we have a a window to treat the same patients with Claude Strom. But more importantly, Claude Strom is a is a systemic therapy. And as I said in in the the presentation just a few minutes ago, RDEB and indeed all EB is actually a systemic disease. And these kids and and indeed when they get through to adulthood, they suffer the condition throughout their esophageal tract, and they're more widespread than just the the dermis.

Speaker 3

And so we see a role for Cordstrom in treating those patients with systemic disease as well as skin lesions. Indeed, that, you know, a trial of a a similar MSC product that's not going through to license in in in South Korea showed improvement in skin scores, after, 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 presence of of the current licensed alternatives.

Speaker 8

Understood. Thank you for taking the questions.

Speaker 2

And

Operator

now that will conclude the q and a portion. I will turn the program back over to doctor Tessi for any additional or closing remarks.

Speaker 2

Yes. Thank you all for attending today's call, and I'll 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 immune bio and got Xpro in 02/2017 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.

Speaker 2

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. Immune 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.

Speaker 2

Stopping neuroinflammation by immunosuppression, glial suppression, is very different than stopping neuro destructive neuroinflammation by repolarizing glial cells to support the CNS cellular unit and improving remodeling and repair. The goal of effective therapy for the Alzheimer's disease is to reestablish normal glial homo homeostasis. The idea that the brains of the elderly with dementia can undergo remodeling and repair is novel. We believe data from the MINDFELD trial will change the direction of scientific research and discovery in the neuro neurology and CNS drug development arena. I've said before that this is the dawn of the golden age of CNS development.

Speaker 2

We believe it is, and we look forward to leading the charge. So with that, I thank you, and I'm we will be talking to you all soon when the data are released. So thank you very much.

Operator

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

Powered by Quartr

Key Takeaways

  • Immune Bio expects to report top-line results from its Phase 2 MINDFUL trial in early Alzheimer’s disease in mid to late June, with EMAC and p-tau217 among key endpoints.
  • New biomarker data presented at ADPD suggest that over two thirds of early AD patients are APOE 4 carriers, boosting the addressable market for Xpro to ~70% versus the previously cited 40%, and highlighting an unmet need in APOE 4 homozygotes excluded from current anti-amyloid drugs in the EU/UK.
  • EXPAREL (Xpro) has shown an excellent safety profile in elderly, comorbid early AD patients, with no serious CNS adverse events, unscheduled MRIs or deaths reported to date.
  • In the pipeline, CordSTROM for recessive dystrophic epidermolysis bullosa has received Rare Pediatric Disease and Orphan Drug designations and is on track to file a BLA in 2026, while the Inkmune prostate cancer trial continues enrolling Phase 2 patients with immunologic and PSMA PET data forthcoming.
  • As of March 31, 2025, Immune Bio reported a Q1 net loss of $9.7 million and held $19.3 million in cash, providing a runway through Q3 2025; upcoming catalysts include the FDA end-of-Phase 2 meeting for MINDFUL and initiation of a Phase 2 trial of EXPAREL in treatment-resistant depression.
A.I. generated. May contain errors.
Earnings Conference Call
INmune Bio Q1 2025
00:00 / 00:00