INmune Bio Inc.

Ladies and gentlemen, greetings and welcome to the Immune Bio fourth quarter 2023 earnings call. At this time, all participants are in a listen-only mode. A brief question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star and zero on your telephone keypad. As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it is my pleasure to introduce Mr. David Moss, CFO of ImmuneBio. David, the floor is yours.

Thank you, Ryan, and good afternoon, everybody. We thank you for joining us for the call for ImmuneBio's year-end 2023 financial results. With me on the call is Dr. RJ Tessie, CEO and co-founder of ImmuneBio, and Dr. Mark Lodell, Chief Scientific Officer and co-founder of ImmuneBio, who will provide an update on IncBio, our memory-like natural color cell oncology platform. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those such as forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release, as well as risk factors in the company's SEC filings, including our most recent quarterly 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 the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, Immune Bio disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. Now I'd like to turn the call over to Dr. R.J. Tessie, CEO of Immune Bio. R.J.? ?

Yeah, thank you, David, and thank everyone for joining the call. As usual, I will arrange my remarks to highlight the key takeaways for the fourth quarter and the subsequent period and provide updates on our platform programs. I will start by reviewing developments on our EXPRO platform and then pass it over to Mark Liddell, who will provide an update on Incmeon. David will conclude with a discussion of our final results. and providing an update on upcoming and new milestones. During the fourth quarter in early 2024, there were several positive developments in our phase two trial in patients with early Alzheimer's disease. First, we received acceptance of our clinical trial application by several EU countries to allow us to initiate the phase two trial in those countries. Clinical trial sites in Poland, Spain, France, Czech Republic, and Slovakia will soon be enrolling patients. The UK continues to be very active in recruiting patients for the phase two trial. And the UK is ideal, an ideal jurisdiction to expand or to develop our program because it possesses one of the highest rates of Alzheimer's disease in the rest of the world, coupled with a robust for-profit medical research infrastructure. Patient enrollment tends to be faster in the private for-profit sites compared to academic or government-run hospitals. The FDA lifted the clinical hold for the AD program in January of this year. We have previously announced we will not be enrolling patients or adding trial locations in the U.S. This is a simple issue of timing. The time and cost to open U.S. sites is such that we probably would not be successful getting any patients enrolled before the phase one and phase two, excuse me, enrollment is completed. That cost just can't be justified. We expect no U.S. patients to be enrolled in this trial period. We are often asked if this strategy will compromise the expo development program in Alzheimer's disease. The answer is a loud no. There is no requirement that U.S. patients be included in any drug trial. The FDA's preference for including U.S. patients in clinical trials is due to demographic considerations, not due to doubts about the validity of non-US clinical trial results. Although the FDA has issued guidance recommending that clinical trials reflect demographic diversity of the US population, this goal has not been achieved in the recent pivotal trials for the anti-amyloid treatments. We expect the US will be a key jurisdiction for clinical trials and patient enrollment in the pivotal AD trial that will follow this trial. One of the realities of a six month clinical trial is that phase three planning must begin well before patient enrollment in the phase two trial is complete. Our goal is to complete end of phase two meetings with the FDA and other regulatory authorities in mid 2025 to get a clear outline of what would be required for an approvable phase three trial. Discussions of patient diversity in the U.S. cohort will be had at that time. This does not mean we are not in communication with the FDA on ex pro for Alzheimer's disease. We plan to submit for accelerated approval pathways for ex pro in Alzheimer's disease. The first submission will be a fast track pathway. Then once we have compelling phase two human data, we will submit for breakthrough status. Recently, in fact, a month ago or less, the FDA released draft guidance on the development of drugs for the treatment of patients with early and prodromal Alzheimer's disease. The guidance supports many of the strategies we have been including in our trials, including enrichment and novel endpoints. The guidance also provides direction on how to think about prevention of Alzheimer's in patients with prodromal disease. This is something we think EXPRO will be very good at and we will be talking about more in the future. I want to take a moment to address two unique elements of our Phase II clinical trial, the endpoint and the six-month duration of the trial. We are often reminded that we do not look like, excuse me, that we look different than the gold standard set by a big pharma in their anti-amyloid trials, but looks can be deceiving. A look below the surface shows many similarities between those large and long trials and our trial. Despite all of the talk about EMAC as our primary endpoint for ADO2, the trial is powered on CDR. CDR is a well-accepted cognitive endpoint used in all of the anti-amyloid trials. In fact, let's compare our trial with Expo for the treatment of early AD with the positive phase three trials that use the anti-amyloid drug for the treatment of early AD. The three trials have two things in common, the use of CDR and a six-month trial time point. Both the Canumab and Donamimab phase three trials showed statistically significant advantages of the anti-amyloid treated patients compared to placebo at six months. Put another way, both those trials could have been stopped at six months with positive results. The difference seen between the placebo and treatment groups in the anti-amyloid trials is exactly the same difference we expect to see between expro-treated and placebo-treated patients. In summary, we are very confident that the expro trial is well-designed, statistically sound and substantially de-risked. The ex-pro trial looks almost exactly what has been successful with leucanumab and donaminab. In early March, INCME issued a joint press release with Kinos Bioscience, highlighting advanced AD patients who received weekly ex-pro treatment for four weeks had a statistically significant increase in alpha wave frequency and power. Reduced alpha-weight power has been linked to cognitive decline and progression in MCI and Alzheimer's disease. The EEG long considered a gold standard in objectively measuring brain activity provides valuable insight into brain function and neural connectivity. Studies have consistently highlighted a progressive decline in alpha-band power in patients like ours. To our knowledge, we are unaware of reports of drugs in AD development that show consistent decreases in alpha wave power. We believe this is an easily measured biomarker of improved brain function in patients without Alzheimer's disease. But without a roadmap, that is other results, we need to wait for the results of our trial to determine if an increase in alpha wave power correlates with cognitive improvements. Just to be clear, the seven patients in this pilot study are patients with moderate to severe Alzheimer's disease. And so they're very different than those in the early Alzheimer's trial. We sought to evaluate the utility of EEG as a functional biomarker in this group. We believe this is just the beginning, or as we like to say, the tip of the iceberg, of what we can expect to be positive news on Alzheimer's, not only in halting the progression of cognitive decline in Alzheimer's disease, but hopefully in restoring cognitive functionality. This last point is why we're using EMAC. EMAC has the ability to demonstrate improved cognitive function after expert treatment. Standard cognitive measures in Alzheimer's disease can only measure stable or decreasing cognitive function. We like to boast that targeting neuroinflammation with Expro provides many market expansion opportunities into other neurodegenerative and behavioral diseases. Go no further than our website to see 87 publications and more than 12 different diseases where Expro has been effective in clinical models, preclinical models. Treatment-resistant depression, or TRD, will be the first disease beyond Alzheimer's that we've developed. We will be making further announcements on the TRD Phase II trial using EXPRO in the near future. Our goal is to enroll the first patient in this NIH-supported Phase II trial in the second half of 2024. I now pass the mic to Mark Liddell, the co-founder and CSO of ImmuneBio, to update progress on the InCommune program. Before I do so, I and the entire ImmuneBio team want to recognize congratulate Mark for a recent significant achievement. Two weeks ago, we received notice that Mark was awarded a career achievement award in cell and gene therapy by the International Society of Cell and Gene Therapy. The ISCT is the society in cell and gene therapy, and the organization considers this award its highest honors. The award was announced as part of the annual ISCT major awards announcement. And Professor Liddell received the award during the organization's annual meeting in Vancouver on May 29th. We couldn't be happier for Mark and believe this recognition is well-deserved. Congratulations, Mark.

Ladies and gentlemen, the line of Dr. Mark Liddell has been disconnected. Please stay connected while I connect him. Thank you.

Okay. Mark, there's a storm in the UK where Mark is, so

Well, I'll tell you what, I'll go to my part and then we can come back to Mark if you don't mind.

Okay, that's fine. So I hope the audience doesn't mind that, but I think that's the way to go because Mark is really the one that needs to speak about income. So David?

I'll jump on here. And RJ, maybe what you could do is just text Mark so you can get him on the line. So I'm going to provide a brief overview of our financial results and upcoming milestones, and we'll go back to Mark, and then Mark will move on to Q&A. Net loss attributable to common stockholders for the year ended December 31st, 2023 was approximately $30 million compared to with approximately $27.3 million for 2022. Research and development expenses totaled approximately 20.3 million for the year ended December 31st, 23 compared with approximately 17.1 million for 2022. General and administrative expenses was approximately 9.6 million for the year ended December 31st, 23 compared with approximately 9.3 million for 2022. At December 31st, 2023, the company had cash and cash equivalents of approximately $35.8 million. Based on our current operating plan, we believe our cash is sufficient to fund our operations into Q4. As of March 27th, 2024, the company had approximately 18 million shares of common stock outstanding. As highlighted in the prior quarter's investor call, 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. Full enrollment in the Phase II Expo trial for the treatment of neuroinflammation as a cause of Alzheimer's disease are expected mid-2024 followed by top line data approximately six months from the last patient enrolled. We will initiate a phase two trial of EXPRO in patients with treatment resistant depression in the second half of 2024. Cohort one of the metastatic castration resistant prostate cancer program is nearly complete with all three patients enrolled. We expect cohort two to start in April with open label data to follow. We expect to complete enrollment in the phase one portion of the metastatic castration-resistant prostate cancer trial by the end of Q3-24, and the phase two portion is expected to complete enrollment in Q2 of 2025. An upcoming webinar on using Expro to promote remyelination in neurodegenerative disease will be announced in Q2. We encourage you to look out for this event and do your best to try and join. It should be pretty exciting. And then at this point, I think, Mark, are you back on the line?

David, Mark is still not online.

Yeah, so he says he's going to try a web call, but let me go ahead and get started, and he can jump in. So on to IncMUNE. So we apologize for the technical problems.

So we achieved... I've actually joined RJ.

Okay, go ahead, Mark. Mark, I did give your accolades about your awards, so you can start from there.

That's very kind of you. Sorry, everyone. I'm in the UK and we've got a thunderstorm going on and I got dropped out. Anyway, thank you very much, RJ. Of course, I'm very honoured by the ISCT's recognition and obviously pass my thanks to all of my current and former colleagues that I've had the pleasure to work with over the years. It's a great reflection on the entire research effort and success of everyone I've been lucky to work and collaborate with over the course of my career, and I hope it continues. So most notably for us, though, that we achieved a company milestone at the end of 2023, in the last weeks before Christmas, with the launching of the Phase 1-2 open-label trial of INCMUNE in metastatic castration-resistant prostate cancer, or MCRPC for short, with the first patient dosing taking place in the final week at the end of last year. The trial is actually unique in many ways, as seems to be the trend of our company. First, the concept. This is an NK therapy trial that does not give NK cells or use cytokines. IncMune converts the patient's own residual NK cells in their circulation from resting, non-cancer-killing state, to what we now know are memory-like NK cells that are able to destroy NK-resistant cancer cells. So unlike more conventional adoptive immunotherapies with NK cells from donors, patients don't require any type of conditioning chemotherapy, and nor do they require NK-stimulating cytokines, as is common to other NK-activating therapies. Incline patients sitting in a chair as an outpatient can get an IV or intravenous infusion over 20 minutes and then having received their dose of Incline, they're able to leave. We've given over 20 doses of Incline in an outpatient setting so far. Each infusion was remarkably boring for the patient and as importantly for the clinical team as it appears to be so well tolerated. In each patient in the trial, we're monitoring immunologic endpoints, as you would expect, that include NK cell number, the phenotype of those NK cells, and their ability to kill NK-resistant tumor cells. We also measure tumor-related variables. In this MCRPC trial, we measure anti-tumor effects by following blood PSA levels, tumor volume with PMSA scans, and circulating tumor DNA. So this rich data set will allow us to predict if the therapy warrants a pivotal trial at the end of phase two. The phase one, phase two trial is expected to enroll 30 patients. These men have all received PREMIUS therapy and now have metastatic gastrate-resistant prostate cancer. They received three infusions of INCMUNE as an outpatient treatment, as I said, during that six-month trial. We have three centers enrolling patients, and another five are expected to open over the next few months. The phase one portion of the trial will be completed by September this year. and we expect patient enrolment in the Phase 2 portion to be completed by the second quarter of next year, with data available for all of the patients by the end of 2025 at the latest. It is an open-label trial, and we expect some snapshots of the data in 2024 or in early 2025. Equally importantly, the Equimmune team has been working very hard on perfecting the manufacturing and logistics elements of immune therapy. So when wearing my academic hat over the last 35 years, I've seen many promising therapeutic strategies in the cell and gene therapy space fail due to manufacturing and logistical problems, and you'll all be aware of some of those associated with adoptive immunotherapies like CAR-T. We're scaling up the manufacturing process in preparation for the pivotal trial, and we've perfected the quality and release assays requested by the regulatory authorities. Because the product ships on dry ice, Logistics and storage at treatment centers is easy and fits in with many other conventional drugs. So simply put, we can make the drug, we can ship and store it, and the clinical trials will determine the therapeutic value in this setting. Our pivot from hematological malignancies to solid tumors was not a one tumor project and has been well planned. The unique attributes of ink immune primed NK cells make them ideal to treat a wide variety of solid tumors, and we've published on those. Prostate cancer is the test case, but we found sound preclinical work in ovarian cancer, and we're developing the same data in renal cell carcinoma. So given resources, these will be the next targets of ink immune therapy. So that ends my update on the ink immune platform, and I'd like to turn the call over to David Moss, our CFO, to discuss the financials. Thank you, David.

Well, I appreciate it, Mark, and thank you for the update. Since I've already gone through the financials, in summary, management feels that the company has two great platforms and is a small organization with limited resources. We'll try to expand the application of these platforms when resources allow. We greatly, greatly appreciate your continued belief in our small company and support of shareholders. At this point, I'd like to thank you for your time and attention. I'd like to turn it back to Brian to poll for questions. Brian?

Thank you. Ladies and gentlemen, we will now be conducting a question and answer session. If you would like to ask a question, please press star and one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star and two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Ladies and gentlemen, we will wait for a moment while we poll for questions. Our first question is from Thomas Strado with BTIG. Please go ahead.

Hi, good morning. Good afternoon. This is for Tom. Thanks for taking our questions. So two for us. So first, for the planned study in TRD patients, is there an obvious criteria for patient stratification to enrich for patients who are likely to benefit from XPRO? And then question number two is, so for the recent EEG data that was presented, how established is the correlation between EEG changes and improvements in cognition and memory? Any additional insights would be helpful. Thank you.

Yeah, so thanks. The first question is on TRD. And in fact, we will use CRP. So these patients have had to be confirmed to be treatment-resistant, which means they failed two previous tests. lines of antidepressant therapy, and they need to have an elevated CRP. So we're not adding the other three biomarkers we use in the AD trial, but it's the same principle that patients with neuroinflammation will benefit from Expro. And it turns out that neuroinflammation makes patients resistant to traditional antidepressant drugs. So this is an ideal treatment group for us to treat. Now, I missed the first part of your second question, so ask it again, please.

Just how established is the correlation between EEG changes and improvements in cognition and memory in Alzheimer's disease?

Yeah, good question. In fact, it's not established. As far as we, we obviously did a very deep dive here, and we could only, so we could only find published data on patients with head injury. In other words, if you have a head injury, TBI, your alpha wave declines, And then four weeks later, when you get better, your alpha wave goes up. So there's an improvement in alpha wave in a patient who has cognitive dysfunction after TBI that improves. That is not a drug trial. We looked hard at the drug literature and could find no data that really supports that correlation. And that's why I was saying we don't really have a roadmap. There's a couple, there's some debate with the nethazil, whether it in fact increases alpha wave power in patients that respond. But I would say that's a debate at this point. I would honestly, we believe, and the experts believe that it is consistent with improvement in synaptic function and brain function. We'll see after our phase two trial. We hope it's the case.

And if you don't mind, RJ, I'd just like to add a little bit on the TRD. And I wish we had CJ on the call because CJ is really a TRD expert. But one of the reasons why we're very interested in TRD is that Andy Miller and Jen Felger, two KOLs that are in the space, there was a trial that was previously run with TNF inhibitors. It's a published paper on it. I'd be happy to send it to you. I think it's listed on our slide on the TRD deck. And it shows a failed trial that just took all comers, but it shows that patients that had elevated CRP, elevated measures of neuroinflammation, had a very statistically different result, a positive result when treated. And so if you select your patient population and you use a better TNF inhibitor, i.e. X-Pro, we feel very confident that that is a trial that will be successful. And really, Andy Miller... has really been chomping at the bit to do this trial for many, many years, and that's the reason it's set up and one of the reasons why the NIMH, the National Institutes of Mental Health, gave the company a $2.9 million grant to do that trial.

Thank you for all the detail.

Thank you. Our next question is from the line of Joel Bedding. Please go ahead.

Great. Thanks for taking the questions and for the update today. First question is, as you involve a Phase II Alzheimer's trial, what about the profile of ExPRO or the previous data resonates the most with investigators?

So, yeah. Thank you, Joel. So, remember that this trial is occurring in jurisdictions that do not have the anti-amyloid drugs approved. So, you know, that's Canada, Australia, Europe, and the UK. So in fact, number one, they're excited about the fact that they have something to offer their patients. Number two, you know, they read the literature like everybody else and they, you know, especially those that haven't had hands-on experience with the anti-amyloids, they're just not sure. And here we are giving them a drug that is both safe and we think And we've convinced them it's effective. So they like the safety profile. They like the idea that it is targeting something else besides amyloid. And they also like the idea that the trial is only six months because if, in fact, the patient doesn't respond, then the patient can move on to another clinical trial and still probably qualify where if it was an 18-month trial, that wouldn't be the case.

A question on Inc. Moon with the prostate cancer trial now underway. Can you share anything about the potential cadence of when you might be able to share data from the trial with investors?

Yeah, the best thing I can tell you is that Today, we treated the third patient, so the last patient in the first cohort with the final dose of drug. Obviously, that's the lowest dose, and we will start analyzing those data as they come through. We have got patients lined up now to start the second cohort, so we're right on schedule to deliver this trial on time. believe we will be coming out with good news as it comes through. And I think September is when we will be looking for that, for those dates to come out, because we'll be able to maturely analyze them across the three dose levels. But if we get any remarkable data prior to that, then we'll go public with that.

Thank you.

Thank you. Our next question is from the line of Daniel Carlson with Tailwind Research. Please go ahead.

Hi, guys. Thanks for taking my questions. RJ, you've talked about comparing Expro to the anti-amyloid trials at six months. We know those trials are much larger in size than your Expro trial. What gives you confidence that you'll be successful in comparing them comparing your trial to theirs at six months?

Great question, Dan, and pretty easy to answer. This is where the enrichment criteria come in. You know we've been touting the fact that we only enroll patients with neuroinflammation, and we define that by one of three blood tests or being ApoE4 positive. By doing a trial that matches the patient's disease, neuroinflammation with a mechanism of action, a drug that treats neuroinflammation, you actually make the trial work at six months better than the anti-amyloid trials. That is, to put it in decent terms, the statistical power increases because the variance decreases. So because there's less noise, the data we get is cleaner. So whereas they need It turns out if you look at the results they got, they would have needed about 700 patients per total, so 350 per arm, to actually have a positive trial at six months, but we only need 200. So it's all related to the enrichment criteria. We've always called it a little bit of our secret sauce, and this is a good example of why it's the secret sauce.

Gotcha. That makes perfect sense. Thanks. Mark, question for you on Incmune. The prostate market has certainly heated up in these radioconjugate companies. Some of them have been acquired and some financed things with great valuations, etc. Can you compare or just tell us how Incmune competes with radioconjugates?

Yeah, thanks, Dan. That's a very good question. And plainly, they're much further down the line than we are in their trials and getting their drugs licensed. But the fact is that radiopharmaceuticals are tough to deliver, just getting the isotopes. And if you think about Plavicto, the lutetium-177 that they use for Plavicto, there's only one manufacturer. of lutetium-1717 in the entirety of the United States. And I think there's probably only three globally. So you do end up looking, as we've seen with the strontium-89 in metastron, a challenge in getting the availability of the radio ligand. The other problem, of course, or one of the other problems is, of course, the short shelf life. Lutetium's got a shelf life of, I think, 6.7 days or 7 days. So you're manufacturing lutetium issues are very considerable. And I think as these drugs get more widely used, we're going to see bigger problems with that. But I guess that the real difference is the sort of recall effect that you get, which leads to off-target toxicity, even with these relatively well-tolerated drugs like Blavicto. You've got bone marrow suppression, these patients become anemic. And so that's fine in the metastatic castration-resistant prostate cancer setting, where you've got patients who are very far down the therapeutic line. But it does make them more challenging to deliver earlier in the treatment process. And the great thing about ink muon is its complete lack of toxicity in the patients we've treated so far and in the animal models that we used beforehand. So I think the great difference, if you wanted to look at one now, if we're successful with ink muon, I see it moving earlier in the treatment paradigm. so you end up treating patients with early-stage disease, which is where we are with many of the other immunotherapies. So that's where I think the difference will be. We'll have a wider population of less severely sick patients.

Awesome. That's great. Thank you. That's good input. Thanks. And then one last question. RJ, just if you can comment. Incommune and the Alzheimer's trial, the enrollment seems to be on track. Can you just talk about the trends you're seeing in enrollment right now?

Yeah, well, so I'll start with Incommune. Incommune is actually, enrollment has been constrained by the FDA's requests. In other words, they wanted in the phase one portion of the trial, 28 days between each patient in the cohort. So by definition, the first, you know, getting all three cohorts done will take nine months. Now, there is some speed up because of the Bayesian design, because there is some overlap of the phase two groups. But the bottom line is, we've had more patients actually contacting us who want to be enrolled in the trial than we have slots for right now. Now, knock on wood, let's hope that continues when we get to the phase two portion where we have a little more flexibility in enrollment rates. But the bottom line is, prostate disease is common. The patients are actually quite sophisticated in searching for clinical options. And so they contact us as often as our clinical sites go looking for them, which is quite encouraging. Alzheimer's disease is more interesting, as I said earlier, because all of our studies are in jurisdictions where the anti-amyloids aren't approved. In fact, we're only competing with other clinical trials. Now, there's a lot of clinical trials in Alzheimer's disease, including both companies are running phase threes and, and other trials. So there's a lot of patients being consumed by the anti-amyloid trial. But as I said, uh, to, to, uh, Joel, I mean, the, you know, exposed, it's kind of an attractive drug. It's a different mechanism. So we get a good listen, you know, it's safe. It's a good mechanism. You know, I have to say, it's not, it's rarely the patient that chooses on which trial to be in. If they're really follow the advice of their clinicians, uh, But the clinicians kind of like what we're doing. And so far, so good is all I can say. I will say that we, you know, every day we get up and we think of ways that we can speed enrollment. And I think, you know, I think we've got some ideas and we're pushing hard. And so far, fingers crossed, toes crossed, everything's going to work out as we promised for the last two years, despite our frustrations with the FDA. Okay.

I'd just like to say, Dan, I've been doing early phase clinical trials all my career, and I have never known a trial, either the expert ADO2 trial or our immune trial in prostate cancer that has enrolled to schedule in the way that these two trials have. And so we can be really confident about the outcome, the delivery time point. given the sheer enthusiasm for patients on both trials, which I say is remarkable in my experience.

Well, thanks, guys. I mean, after going through COVID with a number of companies, missing their timelines because of enrollment issues, it's great to see these trends. So thank you for that. Appreciate it.

Thank you. As there are no further questions, I would now hand the conference over to Dr. R.J. Tessie for his closing comments.

Yeah, so thank you. So ImmuneBio is making progress on two fronts, and we're pretty proud of that. I will say the drug development landscape for the treatment and cognitive decline in Alzheimer's disease is really changing rapidly. And we are impressed how quickly the conversation has pivoted from treatment of dementia to prevention of dementia. I can't help wonder if this rapid pivot is because of the satisfaction and frustration with the approved therapies. You know, there's still a niggling concern that the risk profile is not ideal. But I have to say at ImmuneVial, we have a little bit of a different view. We believe the anti-amyloid drugs are chasing the wrong target. We believe neuroinflammation is intimately involved in disrupting nerve cell function and survival and synaptic function. And those are the two essential elements needed for cognitive decline. With EXPRO, we are attacking this pathology and have strong evidence that we changed the biology of the brain for the better. The ongoing phase two trial will allow us to correlate these biologic benefits with cognitive change and we hope cognitive benefits. Stay tuned because the positive result there opens the door to other indications where neuro inflammation meets cognitive dysfunction. Likewise, InCommune is an NK therapy of a different stripe. The biology is sound. It's a lifetime of work by Mark Liddell and he is getting finally recognized for what has been long due. We marvel at the safety profile of this immunotherapy. Could this be a cancer therapy that really has no side effects and only has benefits? Time will tell and we believe the metastatic castrate resistant prostate cancer trial will give the product a good chance to shine. We remain optimistic about both our programs and we thank you for your support and your attention.

Thank you. The conference of immune bio has now concluded. Thank you for your participation. You may now disconnect your lines.