Greetings, and welcome to the INmune Bio Fourth Quarter and Full Year 2022 Earnings Call. This conference will be recorded. A brief question-and-answer session will follow the formal presentation. [Operator Instructions] It is now my pleasure to introduce Mr. David Moss, CFO of INmune Bio. David, the floor is yours.

Thank you, Paul, and good afternoon, everybody. We thank you for joining us for the call for INmune Bio's full year 2022 financial results. With me on the call is Dr. RJ Tesi, CEO of INmune Bio; and Dr. CJ Barnum, VP of Neuroscience, who together will provide a business update on our dominant negative TNF platform, or XPro. Also on the call is Dr. Mark Lowdell, Chief Scientific Officer of INmune Bio, who will provide an update on INKmune, our memory-like natural killer 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 in such 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 of the date they are made as of the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligations to update these forward-looking statements to reflect future information, events or circumstances. Now, I'd like to turn the call over to Dr. RJ Tesi, CEO of INmune Bio. RJ?

Yeah. Thank you, David and I thank everyone for joining us today. As usual, I will arrange my remarks to highlight key takeaways from the fourth quarter and provide updates on our platform programs. I will start by reviewing our developments in XPro, CJ Barnum, the VP of CNS Development, will help me with those comments. I will then hand it over to Professor Mark Lowdell, our CSO, who will focus on what's going on with the INmune program before I pass it back to David to go over the financial results and provide an update on upcoming and new milestones. This will be followed by a Q&A. I will begin with our Phase 2 program in Alzheimer's Disease. Actually, ADi is what we call it, Alzheimer's Disease due to inflammation. We continue to enroll patients in the U.S. and Canada. The FDA's full clinical hold has affected our timelines. This has encouraged us the company to develop alternative strategies to meet our primary goal of completing the Phase 2 Alzheimer's program in a timely fashion. We have implemented several important changes in the last few months to help us reach that goal. We will modify the enrollment criteria in the larger longer Phase 2 mild AD trial to include both mild AD and MCI patients, mild cognitive improvement patients. As you know, they're kind of a prodrome for Alzheimer's. So adding the MCI patients is a new change. This consolidates the MCI and the mild Alzheimer's disease trials into an early Alzheimer's disease Phase 2 study. As you recall, we had separated them previously into separate trials. The combined trial should improve our ability to demonstrate a clinical benefit in patients receiving XPro should accelerate enrollment and reduce costs. The consolidation should help us achieve our goal of reporting…

Thanks, RJ. As RJ mentioned, the AD02 Phase 2 trial, a mild Alzheimer's patients with inflammation is open in Australia and Canada. As a reminder, ADO2 is a blinded randomized placebo controlled study evaluating cognition in mild AD patients and biomarkers of inflammation. We have started the process to include MCI patients also with biomarkers of inflammation into that trial. This complex regulatory process is underway. Once complete, this trial will enroll early AD patients, a group that includes both MCI and mild AD patients. These patients will be treated with XPro for six months. Including MCI patients has two important benefits. First, it improves our ability to observe a clinical response as our expectation is that XPro will have a greater benefit in MCI patients than in even mild AD patients. This is further driven by extending the treatment of MCI patients from three months as we were in AD03 to six months of treatment. With longer therapy, both the number of MCI patients responding and the magnitude of that response should be greater. Second, our clinical sites have told us that including MCI patients increases the number of eligible patients for the trial and should positively impact enrollment. Importantly, consolidating trials allows us to save costs by treating fewer patients in a single trial. The primary reason we had to separate studies, we had two separate studies for MCI and mild AD were based on the MRI biomarkers of primary interest, not clinical outcome. As you may recall, the primary endpoint for both AD02 and AD03 is the EMACC, a cognitive composite that was empirically derived to measure clinical, cognitive changes during early AD. As it relates to the differences in imaging biomarkers, we will address these differences by pre-specifying the expected change in MCI in mild AD patients. Patients that complete the six month Phase 2 early ADi study are eligible to enroll into a 12-month Open Label Extension trial or OLE. The OLE study is a 12-month study where safety and efficacy of XPro will continue to be evaluated. Efficacy will be assessed every three months by MRI and clinical rating scales. All patients that enroll in the OLE study receive XPro regardless of previous treatment assignment. The OLE serves multiple purposes. First, it provides long term safety data. We believe regulatory authorities will expect 18 months of safety data for marketing authorization. The OLE strategy will provide this critical safety data. Second, the OLE provides long-term efficacy data. Third, the OLE is a recruitment tool, guaranteed access to 12 months of treatment following a six month study provides significant advantages over other trials. Patients and clinical teams like this trial design and so far patient participation in the OLE is high. We expect to share some of this data in due time. Now, I'd like to pass the call back to RJ.

Thank you, CJ. I will now move to INKmune, our memory-like natural killer cell priming program. The high risk MDS/AML INKmune Phase 1 program continues to make progress in the UK with the second site now open at the Royal Hallamshire Hospital at Sheffield University Medical School. A patient was consented this week and will -- treatment is planned on for March 7, a week from today, excuse me, March 9, a week from today. In addition, we will also be expanding the MDS/AML program into Europe with a third site Attikon University Hospital in Athens, Greece is expected to open later this month. We've previously stated that INKmune may be an ideal therapy to treat solid tumors because of its performance in the hostile environment of the TME. Mark Lowdell will discuss this more in a moment. In October, we announced positive solid tumor pre-clinical data and prostate renal cell, ovarian in nasopharyngeal cancer cell tumor lines that tumor lines that are all resistant to NK killing that when the NK cells are treated with INKmune, they now can kill these NK resistant tumors. We implied we were pivoting to solid tumors because we thought the effects of INKmune were somewhat unique. And today we are pleased to announce that the company will be filing for an IND to use INKmune to treat patients with metastatic castration-resistant prostate cancer in the US. Prostate cancer is the most common cause of cancer in men, if you excludes non-melanoma skin cancers. The trial is expected to take place in four or more medical centers in the U.S. It will enroll approximately 30 patients in a flexible bayesian design that will allow us to determine safety, proof of biology and confidently picked the dose of INKmune to move into a blinded randomized potentially pivotal trial. As you have come to expect, we are using a mix of standard and novel biomarkers to measure tumor response, when finished, we should have a good understanding of how the drug works in the disease and have a credible biomarker package to move into the blinded randomized trial. If I can paraphrase the quote from Professor Matt Rettig, the Principal Investigator from the Jonsson Comprehensive Cancer Center at the UCLA School of Medicine, “there is no -- there are no good options for metastatic castration-resistant prostate cancer, especially given the recent failures of checkpoint inhibitors.” We are excited about the potential of INKmune in treating solid tumors and hope to make a difference in men with prostate cancer. With that, I'll pass it to Professor Mark Lowdell, CSO. Mark?

Thank you, RJ, and thank you once again to everyone that's joining us to hear. What I think are some really exciting progress that we've been able to make. So you will know that we recently shared with the investment community positive solid tumor efficacy data with INKmune in multiple cancer cell lines as RJ alluded to. And as we highlighted in our recent press on the topic, solid tumors are the majority of human cancers, I'm sure you will know that, but cell therapies currently focused on the 10% hematologic (ph) or liquid cancers. The recent data that we've shown and shared with people provide insights into why the company believes that in INKmune [Technical Difficulty] killer cells to override the immersive hypoxia and regulatory cells in the tumor environment or the TME for short. The interaction of the TME with cancer cells enables can drive tumor progression and that's well known. And it's thought to prevent many cell therapies from being effective and we've seen that increasing over the last few years. These complex interactions have to be considered when designing cell therapies to treat solid tumors. And the TME is hostile to cell therapies because of these two things, the presence of the immunosuppressive immunoregulatory cells and the extreme hypoxia or lack of oxygen within the tumor. So a cell therapy to be effective must operate in that tumor environment. And what we've shown over the last 12 months and more recently, INKmune converts resting normal NK cells in patients into what are now known in the field as memory like NK cells and these can target solid tumors directly even in the presence of immunosuppressive regulatory cells as we've shown and particularly in hypoxic environments. The company's preclinical data with human NK cells and cancer cells…

Thank you, Mark. So we kicked off 2023 with our heads down focused on continuing to expand and advance our existing and contemplated trials in the ways that we can manage our resources, including our costs, and our goals to get drugs approved that make a difference at the bedside. Dave will touch on the financial issues later in his remarks. As we enter the second quarter, the conference and events calendar comes back to life. We will be attending the annual AD/PD conference, the largest AD/PD medical event in Europe the last week of March. April, we are presenting two abstracts at the AACR on our MUC4, the role of DN-TNF targeting, MUC4 expressing tumors as part of combination therapy. INB03 is the product that is part of the DNT oncology branch of the XPro platform that we have designated for our oncology activities. In July, AAIC, the Alzheimer's Association International Conference in Amsterdam will be the center of the AD world. We will be there providing insights into that infection diseases do not include amyloid or tau. As you might expect, we are frequently asked about the FDA hold. We continue to work closely as the FDA works to resolve issues that are unique to the FDA. We continue to enroll patients in Australia and Canada and are focused on how we can accelerate our core Phase 2 program in early AD in venues outside of the U.S., that will be beyond Australia and Canada. To be clear, the problems we are facing with the Phase 2 program will not compromise the potential of XPro long-term in Alzheimer's disease. We expect the U.S. will open in time to include Phase 2 patients in the current trial. And we fully expect the U.S. will be a very big part of any successful global Phase 3 registration program for XPro in early AD. We are planning for success in early AD and beyond in diseases like TRD and the many other CNS diseases where XPro will have value. At this point, I will turn it over to David Moss, our CFO to review financial items. David?

Thank you, RJ. 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 year ended December 31, 2022 was approximately $27.3 million compared with approximately $30.3 million for 2021. Research and development expense totaled approximately $17.1 million for the year ended December 31, 2022 compared with approximately $20.5 million for 2021. General and administrative expense was approximately $9.3 million for the year ended December 31, 2022, compared to $8.8 million for 2021. As of December 31, 2022, the company had cash and cash equivalents of approximately $52.2 million. I'll remind everyone this does not include the recent $6.4 million we received in early Q1. Based on our current operating plan, we believe our cash is sufficient to fund our operations into the second half of 2024. As of March 2, 2023, the company had approximately 17.9 million shares of common stock outstanding. I'd like to highlight that for 2022, we sold only 82,900 shares that went only to insiders. As RJ previously mentioned, we are focused on achieving our research and trial programs objectives while remaining prudent on costs. To that end, we estimate that the consolidation of the AD and MCI trials will reduce the forecasted budget outlay for the two combined trials by approximately $8 million. Further, as we continue to dialogue with the FDA, our budgeted spend in the U.S. is not occurring as forecasted thus resulting in less capital outlays. As previously pointed out, our cash burn has been less than budget because both the delay in starting the trials in the U.S. in tandem with the broad-based strength of the U.S. dollar, reducing foreign costs and particularly in Australia. Further, we were pleased to report last month the…

Thank you. We will now be conducting a question-and-answer session. [Operator Instructions] Thank you. Our first question is from Jason McCarthy with Maxim Group. Please proceed with your question.

Hey, guys. Thanks for taking the questions. First question on INKmune, as it relates to your mention of several solid tumor types where it seems to be effective, but you've chosen to go to metastatic castration-resistant prostate cancer. I'd like to know what prompted that decision? And as a second part to that question, this space is a very defined treatment paradigm and kind of where does this fit in or where are you targeting when you think about things like Xtandi and then kind of salvage chemotherapy. We've just seen pluvicto is out there now and Merck just the other day pulled the plug on KEYTRUDA and Xtandi combination?

Yes. Thanks, Jason. So in our minds, a choice -- and we didn't make this alone. We worked closely with the experts in oncology on this decision. The choice is pretty clear. And it's really based on what you just said there are no effective immunotherapies for patients with metastatic castration-resistant prostate cancer that have failed an androgen therapy of some sort and the enzyme, the various inhibitors. So these patients kind of go into a status of dealers choice at many institutions. And although, chemotherapy is often used, the patients can often be elderly. It's not a great choice for them. And quite frankly, they don't work. So what excites the people we're talking about is the fact that you may have an immunotherapy, which, as you know, every other tumor that has had an effect of immunotherapy, there's been difference in survive. Prostate cancer doesn't have one, is INKmune it? Well, the preclinical data suggests it. But we will have to do this randomized trial or this trial, this multi-step trial to actually determine they think INKmune is an adequate therapy. The second reason we like prostate cancer is, as you know, we're kind of the king of the biomarkers and prostate cancers, particularly metastatic castrate resistant prostate cancer has a lot of very informative biomarkers. There's the traditional biomarkers, PSA in the blood, the CT scan and bone scans. But there are some developing biomarkers that are much more interesting for understanding tumor driven burden, including circulating tumor DNA and the PSMA PET scan, which helps you quantify residual disease. This gives you really quantitative evidence of disease status in which way it's been. So we like castration-resistant prostate cancer. We think it's quite a large opportunity that's growing in size and quite frankly, the competitive landscape out there is not well defined because most -- almost every region of the country treats the disease there.

Can I just add -- sorry, I didn't -- I interrupted?

Absolutely. No, I'm done. Go ahead, Mark.

No. I was just going to say, one of the things that frustrates me as someone who trained as an immunopathologist is a lot of the attempts at immunotherapy are based upon a natural assumption that T-cells are the king of cancer immunotherapy and yet as my old boss said to me over 40 years ago, you should go and look at the patient. If you look at sort of publications of the cells that are infiltrating prostate cancer, and the infiltrates that are associated with outcome. It's NK cell infiltrates, not T-cell infiltrates, and checkpoint inhibitors that have beaten you so far don't target any NK cell function. So what we're effectively giving, if you like, and I wouldn't use this sort of lightly, but we're giving NK checkpoint inhibitor immune takes the resting NK cells that are in the tumor and hopefully we’ll pump the way that they do in the lab. So yeah, I think what we're looking at here is going for a tumor where there is good evidence from public literature that the number of NK cells that are there. And the type of NK cell is potentially prognostically valuable. So that's another good reason for prostate cancer.

Got it. And just shifting gears to the Alzheimer's side, if you enroll all the patients in the AD trial before you get off clinical hold? Does it hurt any standing with the company and the FDA?

Good question. The answer is absolutely not. I think, I've been clear that we will -- we're going to have to do a Phase 3 trial. The Phase 3 trial will look -- we assume is going to look very similar because of what this Phase 2 trial looks like. So it will be a global trial that will include obviously North America, Europe and parts of Asia. So the U.S. will be a very big part of that. So there will be -- there's absolutely zero risk that even if we enroll every patient as outside the U.S. that will compromise our ability to move forward.

Okay. Are you selecting countries or more international countries for this trials? So it does set the stage then for…

Yeah. Absolutely. I mean, all of the countries we're selecting would be countries that you would have on your list for a global regulatory Phase 3.

And just like -- I just brief your last question if you combine or when -- as you are combining the MCI and mild AD trials and so one, “early AD trial” how does it not increase the trial size or what will the total trial size end up being now?

Yes. CJ, why don't you go ahead there?

Can you hear me?

Yes.

So it's a good question. Really, I mean, it comes down to when you're powering the study and what your assumptions are. So the assumptions that MCI patients will perform better than even mild AD patients. So when we do that power calculation, we actually increased our likelihood of seeing a positive result on the EMACC. Now it's going to treat -- we believe it's going to increase the trial size a little bit. But we're talking 10, 20 patients, not talking 100 patients.

So the total size would be [indiscernible] range.

So it's 20-ish (ph), I mean, about that. Don't hold us to that number, but that's the kind of magnitude we're looking at. It's not adding the two trials together. It's not 204 plus 60. It's 220. Okay?

Got it. Okay. Great. Thank you, guys.

Yes, just to reinforce what just to reinforce what CJ said, remember, the trial power comes from the difference between the treatment arm and the placebo arm. And the kind of the unsung hero here is that by taking -- doubling the length of the MCI trial, as CJ said in his comments, means you get -- we anticipate more response in the MCI group. So you will increase that delta between the MCI treatment group and the placebo group and that -- and only good things happen when you do that.

Got it. Thank you guys.

Thank you. Our next question is from Tom Shrader with BTIG. Please proceed with your question.

Good afternoon, and thank you, Mark for asking or answering my big question about why castrate-resistant prostate cancer because that's a tough one. And another one, I wanted to ask about the new program in DMD. You commented that there's a little bit of a historical issue with conventional TNF scavengers, the XPro might get around some of those issues. I think you mentioned cardiac-tox. I would ask, how derisked is that idea or the XPro gets around it or would a partner need to do some work to show that this is no longer an issue. And then I have an AD question later on?

Yeah. So I think that's an excellent question. Let me give you the derisk, and then I will give you an educated guess on the -- on whether a partner's going to have to this specific issues. So what happened when they used the original non-selected TNF inhibitors in mouse models, in mouse models to treat DMD. There -- long term, there was a decrease in cardiac output in the mice. Now remember, patients and animals with DMD actually see a decrease in cardiac function over time. It's part of the muscular effects of the dystrophin abnormalities. But actually the TNF inhibitors made it worse. So that basically they just stopped. And what I found pretty interesting from the literature if they stopped and this literature is kind of old, let's call it, early 2000s. They stopped because they became contented with the results they were getting with corticosteroids, right? So the reason we're quite confident that this is not going to be an issue because of selective nature of soluble TNF. We have one published paper that shows in a model of exercise induced atrial hypertrophy in mice that actually XPro decreases hypertrophy and decreases the fibrosis. Fibrosis as part of the pathology of DMD. And we have unpublished data in another cardiac model that shows that XPro, you should see that data probably midyear, that XPro has benefit on cardiac disease. So in fact, we have pretty good evidence in animal studies that XPro is actually beneficial to the heart. And we are soon completing a six month DMD study in the mice where the primary endpoint is cardiac output. So at that point, I'm pretty confident we'll completely derisk it. Now does this mean that when someone takes this and drops it into kids, are they going to have to somehow derisk it beyond the standard clinical trial perspective. I don't think so, but because of the benefits of the drugs that are beyond just anti-inflammatory, but I would rather wait until we ask someone, hopefully a partner actually talks to the FDA. But the bottom line is, our data in cardiac with XPro is quite positive. We will have really unequivocal data based on the animal models quite soon, but everything is pointing to that should not be a problem and the fact that XPro actually improves cardiac function in most disease models.

Got it. Thank you. And maybe probably a CJ question. I understand you want to get XPro approved as a standalone therapeutic in Alzheimer's disease. But it's increasingly clear that ARIA is neuroinflammatory process associated with the A beta antibodies. Have you thought about trying to get a signal to reduce ARIA in an A beta model or in a small trial? Is that a reasonable way to think about getting a quick signal that I think a lot of people would be interested in?

I think we've said previously that’s something we think -- we agree with you. And we think about all sorts of things, not just ARIA, but across the board. And we think XPro is going to be an excellent drug for combination therapy in general. So I guess the answer to your question is yes, we thought about it quite a bit, we thought about a lot of things and hopefully in the near future as we get going in our programs here we can start entertaining them a little more.

Yeah. Tom, RJ here. I mean, that's that is obviously a question we talked about a lot. We have done a bit of a deep dive. There is no -- to our knowledge, and if someone has one, please contact us. To our knowledge, there's no rodents, rat or mirroring model of area. In other words, if you give an anti-amyloid drug to a rat or a mouse, nothing happens. To our knowledge, the only area model is a spontaneous area model in a some strain of monkey, which is not one of the standard strains. And these animals are extremely rare. So it's not like we could just buy a bunch of monkeys, give them an anti-amyloid drug and see who develops area and then treat it because that would be the fastest way forward. We have some ideas. We're talking to people, but we believe we agree with you that the Achilles Heel of the anti-amyloid strategies aside [indiscernible], if I can be snarky, besides the fact that they only work somewhat versus well. They only work somewhat is their safety signals associated with ARIA. And I think that moving forward, people will be a lot more comfortable using a drug with its efficacy profile. If the safety profile can be solved. So it's on our radar screen and stay tuned.

Great. Thank you.

Thank you. Our next question is from Daniel Carlson with Tailwind Research. Please proceed with your question.

Hi, guys. Thanks for taking my questions. Just a quick one on the timeline for the AD MCI trial. Does the second half of 2024, do you need U. S. approval at some point to reach that timeline or is that based on just what you have going on?

So thanks, we've -- I hate to say this, but we're quite confident we're going to be off. We'll solve the FDA problems this year and so we'll include patients. But the more successful we are in getting sites up and running outside of the U.S. and how fast they enroll some of these areas we're looking at are historically quite rapid enrollers, dictates whether it's going to be midyear or later in the year. So at the end of the day, it's going to be 2024. It's going to be the second half. Don't let us get a little farther on, and there will be U.S. patients in that -- in the Phase II trial. It's just -- I don't want to give you what the percentage will be at this point.

Okay. Fair enough. Thanks. And then CJ had mentioned that you're going to get some data from the open-label extension, you said in due time. So I was wondering if you could just sort of tell us what to expect from that? And I was curious in particular if you're measuring cognition in the open-label extension, if we'll get a chance to see that at some point.

CJ?

Hey, Dan. So yeah, so we will be measuring all the clinical rating scales that we have in the AD02 study will be continued in the open-label extension study. So we'll get those every three months along with MRI data. Like I said, our intention is to share that data, but I don't have a timeline as to when we'll see that at this point.

And an interesting problem, Dan is since the Phase II is blinded, we actually won't know if a patient has been a placebo patient or an active patient. So suddenly, they show up Day 1 on the OLE, right? They could be a de novo patient or they could be someone who's already had six months of therapy. So it's not like we're going to know in the first month or two, what's going on. We're going to need some time to figure this out. But it -- remember the three values or the three important elements of the trial of the OLE that CJ mentioned. One, it gives us that long-term safety data that we know the regulatory authorities, one. Two, it gives us the long-term efficacy data that we know the regulatory authorities were going to want. And the third thing is its trade date, what I mean trial date rather. In other words, we're trying to encourage clinical teams to enroll their patients. We know it's competitive out there. One of the great advantages of the XPro trials being only six months is that even if you end up on the placebo trial, your progression rate is not going to be so catastrophic that you potentially can't benefit from some other clinical trial. You don't become un-enrollable, so to speak. And if you do participate in the trial, you're guaranteed to get what we think is going to be a beneficial drug after the period of that trial, whether you're on placebo or not. So we -- the investigators have been very supportive of this strategy because at the end of the day, when you walk into a memory clinic now, they've got three or four or five trials that they can choose between to enroll their patients and they're always trying to look out for the best wishes of their patients, and we think this puts us high on the list.

Yeah. And then one last question, just -- I've just looked briefly since your press release, but your PI and the INKmune prostate trial seems to be a pretty big deal. I'm just wondering what his motivation was to work with you guys on this?

Well, I'll let you ask -- I'll let you -- I don't want to put words in his mouth, but this is, as you said, he's a very experienced guy, clinical trialist. He has particular insight and expertise in immunotherapy. And I think he's just -- my sense is, he's been frustrated that all of his other buddies in the cancer world, whether you're lung cancer or melanoma docs, have all these interesting immunotherapy tools to use checkpoint inhibitors, ADCs, etcetera. And he doesn't have anything, right? And he states that we've reached the limit, I think this is in his quote in the press release, we've reached the limit with what we can do with the effective therapies we have, and those are inhibitors, anti-androgen strategies and chemotherapy. So he believes that the only way he's going to progress is with an immunotherapy. And Mark, you heard Mark's comments, Mark convinced him that what they really need is a therapy that targets NK cells, and he's on board. So we're pretty excited. He's a very good guy. But he's been there, done that, and he's been involved in every immunotherapy failure in prostate cancer going forward because that's what the field has been focused on. They're trying to replicate the success they've had in breast cancer and in lung cancer with immunotherapy in prostate cancer. And so far, it's been a disappointment.

Thank you. Thanks for your answers guys and looking forward to a big year from you.

Thanks, Dan.

There are no further questions at this time. I'd like to turn the floor back over to Dr. RJ Tesi for closing comments.

I think you're on mute RJ?

Well, okay. Thank you. So thank you, everyone for participating in the call. We continue to make progress despite the regulatory challenges and the dislocations in the capital markets. We believe we have novel products that will be valuable to clinical teams and have a broad variety of clinical applications, and you're beginning to see that. And we aren't afraid to innovate in our clinical, regulatory and financial activities. INmune Bio has this can-do attitude that we think will benefit patients and investors alike. And I personally will put Alzheimer's disease and prostate cancer on notice. We're coming after you. So with that, we will close, and thank you very much.

This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.