Inmune Bio, Inc. Q4 FY2020 Earnings Call

Greetings, and welcome to the INmune Bio Fourth Quarter 2020 Earnings Conference Call. 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, Co-Founder and CFO of INmune Bio. David, the floor is yours.

Thank you, Rob, and good afternoon, everyone. We thank you for joining us for the call of INmune Bio's fourth quarter 2020 financial results. With me on the call is Dr. RJ Tesi, CEO and Co-Founder of INmune Bio, who will provide a business update. Before we begin, I remind everyone that except for statements of historical fact, 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 is no assurance of any specific outcome. Undue reliance should not be placed on the forward-looking statements, which speak only as of the date they are made as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligations to update these forward-looking statements to reflect future information, events or circumstances. With the forward-looking statement behind us, now I'd like to turn the call over to Dr. RJ Tesi, Co-Founder and CEO of INmune Bio. RJ?

Thank you, David, and thank you, everyone, for joining the call. I will arrange my remarks to highlight key takeaways for the fourth quarter, year-to-date, and provide updates on our platform programs before I pass it back to David to discuss our financial results and upcoming milestones. Then we will move to Q&A. I'll start with our DN-TNF platform, beginning with XPro1595, which we are developing for Alzheimer's disease and other CNS indications where neuroinflammation plays an important role. The clear highlight since our last quarterly update was data we reported on January 21 from our phase 1 trial of Xpro in patients with Alzheimer's disease. INmune Bio's data-driven hypothesis is that neuroinflammation results in synaptic loss and neurodegeneration, which is nerve cell death in patients with Alzheimer's disease. Synaptic loss and neurodegeneration are the causes of cognitive decline in these unfortunate patients. Finally, we believe the control of neuroinflammation by XPro1595 will help repair synaptic dysfunction, decrease neurodegeneration, and prevent the progression of cognitive decline. Last July, we announced interim data demonstrating that Xpro1595 reduced neuroinflammation by an average of 40% in the arcuate fasciculus, a white matter tract important for learning and memory in patients with Alzheimer's disease. Neuroinflammation was assessed using MRI to measure white matter free water, a validated biomarker of neuroinflammation. The small preliminary data set included six patients, three in a low and high dose group treated with Xpro for 12 weeks. As a reminder, the phase 1 trial is a neuroinflammation trial in patients with Alzheimer's disease. At that time, based on the quality of the data, we committed to initiating a phase 2 clinical trial in Alzheimer's disease by the end of 2021. We remain committed to that goal. On January 21, we provided additional data from nine patients who completed the 12-week treatment period with XPro1595. The group included the original three patients who received weekly subcutaneous injections of 0.3 milligrams per kilogram of XPro1595 and six patients who received 1 milligram per kilogram once a week. These are the low and high dose groups, respectively. We wanted to accomplish two goals with the data release in January. First, we wanted to connect the dots between white matter free water measured by MRI, a validated but new biomarker of neuroinflammation, with traditional biomarkers of neuroinflammation, namely CSF cytokines. The second goal was to determine if the downstream consequences of decreasing neuroinflammation in this small group of intensively studied patients mirrored what was seen in the extensive animal data using external models of neurodegeneration. To accomplish the first goal, we used the O-link platform to measure 47 inflammatory chemokines and cytokine levels in the CSF of patients; CSF, by the way, is Cerebral Spinal Fluid obtained by lumbar puncture; but to measure those levels in the CSF of patients before and after three months of XPro1595 therapy. The cytokines all decreased significantly. For example, CCL2—excuse me, CCL7, a chemokine that mirrors what happens with soluble TNF, decreased by 47% after 12 weeks of XPro therapy, and you can see this in the slide. The decrease in the white matter free water and the decrease in the inflammatory chemokines and cytokines correlated closely, and you can see that the R squared value is greater than 0.7, which is a highly statistically significant correlation despite a small number of patients. What this means for the future is that using MRI to measure white matter free water, at least when looking at neuroinflammation, may be able to replace CSF and lumbar puncture. That's what the future holds. The results presented so far have really met the primary goal of the phase 1 study, that is to demonstrate that XPro1595 decreases neuroinflammation in patients with Alzheimer's disease. We've clearly shown this. Now on to the second question. The second question is, what are the downstream consequences of decreasing neuroinflammation in patients with Alzheimer's disease? We used two biomarker platforms to provide insight into the consequences of the decreasing neuroinflammation. The first was Proteome Bioscience's TMT calibrator to study the changes in the CSF proteome in the Alzheimer's patients before and after 12 weeks of XPro therapy. This is a big data analysis of the CSF proteome that revealed that decreasing neuroinflammation led to a significant change in multiple Alzheimer disease related pathways, including the immune inflammatory response pathway, the CNS neuronal function and injury pathway, and the dendritic spine morphogenesis synaptic plasticity pathway. Notably, the analysis found an 80% decrease in neurodegeneration markers such as neural filament light chain and visinin-like protein 1, and significant changes in connectin 2 and neurogranin, both proteins associated with neuroplasticity. To get a drug approved in Alzheimer's disease, you must demonstrate that the treatment decreases the rate of cognitive decline compared to placebo. This trial does not attempt to meet those standards as a primary endpoint. It's a small open-labeled dose escalation trial, but there is important information included in the data set. The data, albeit preliminary in nine patients, showed that only one patient had progression of their disease during the three-month study. Put another way, eight of nine patients were stable or had improved cognition over the three-month period. Finally, six of the patients, all in the high-dose group, have been enrolled in a nine-month extension study that basically allows them to continue their treatment for nine months after they finished three months on the study. These patients receive safety labs, cognitive testing, and MRI scans every three months. Three patients have already had a year of therapy, and two of these have been approved for a special access program by the Australian government to allow continued treatment of their Alzheimer's disease with XPro1595. We continue to study these patients, and you will hear more about them in the future. In summary, this short trial in a small number of patients clearly shows that XPro1595 quickly decreases neuroinflammation, resulting in positive changes in the CSF proteome and MRI scans using very sophisticated measures that you will see an example of if you go back to the KOL webinar. All of this correlates with what we've seen in animal models. We remain committed to starting a blinded randomized placebo-controlled phase 2 clinical trial in the second half of the year. We have a bit more work to do before we release the precise design of the phase 2 trial, and we continue to enroll patients in the ongoing phase 1 trial and continue to mine the expansive data set that we have and are generating. What we have learned from these patients will prove invaluable as we design the best possible phase 2 trial for the development of XPro1595 in Alzheimer's disease. A second CNS trial we plan to initiate this year is in treatment-resistant depression or TRD. In September, we announced that we were awarded a large grant of up to $2.9 million from the NIH to support a phase 2 trial of XPro1595 in patients with treatment-resistant depression. We will conduct this trial in collaboration with two of the world's pioneers in the field: Professor Andy Miller and Associate Professor Jen Felger, both at Emory University. Dr. Miller is the pioneer in the role of neuroinflammation and depression, having described the problem in the early days of interferon therapy for cancer then going on to publish the first study demonstrating that targeting TNF improves depressive symptoms in patients with elevated biomarkers of inflammation. In addition, Dr. Felger discovered that the connectivity between two measures of the brain, as measured by MRI, that are vital for feelings of pleasure and motivation, are lost in depressed patients with inflammation. Our hypothesis is once again simple: XPro1595 will decrease neuroinflammation, improve clinical symptoms, and restore connectivity between these vital regions of the brain as measured by clinical criteria and by MRI. TRD, treatment-resistant depression, is a neuroinflammation program that leverages a lot of what we're learning during the phase 1 trial in Alzheimer's disease. As with the AD trial, the TRD trial will use biomarkers of inflammation to confirm diagnosis, enroll patients, and determine response to XPro therapy. The use of biomarkers is a novel approach to psychiatric drug development. We believe the use of biomarkers will improve the efficiency of drug development in the field, and we believe we will lead that revolution. Treatment-resistant depression remains an area of significant unmet need. In the U.S., an estimated 7 million patients with major depressive disorder are resistant to current therapies, most often defined as having failed two prior lines of treatment. Current treatment strategies require treatment-resistant patients to cycle through multiple therapies in an attempt to find one that works. We hope to introduce precision into the diagnosis and treatment selection by using biomarkers to identify patients and track their progress. These two programs highlight a key advantage of the XPro1595 platform. XPro decreases neuroinflammation. Neuroinflammation is a key pathology across a number of neurodegenerative and psychiatric diseases. A quick review of more than 60 publications on our website will give you an idea of the breadth of the opportunity for XPro1595 and CNS. Our Alzheimer’s disease and treatment-resistant depression are the first, but not the last of our programs in CNS. Turning now to Quellor, our COVID-19 program for treating cytokine storm. Last quarter, we went into some detail on how cytokine storm lands many COVID-19 patients in the hospital and why we believe targeting soluble TNF as the master cytokine is potentially a more effective approach at suppressing this dysregulated immune response. In November, we announced that the first patient had been enrolled in the phase 2 trial of Quellor for the treatment of pulmonary complications of COVID-19. The double-blind randomized placebo-controlled trial will enroll 366 high-risk COVID-19 patients in two equal-sized cohorts. One cohort is the placebo or the standard of care cohort. The other is the standard of care plus Quellor. They'll be given a one milligram per kilogram subcutaneous injection, and a second dose of Quellor may be given a week later if the patient remains hospitalized. The primary study endpoint—and I will remind you that this trial was written with the FDA, who dictated the design and the endpoints of the trial—is the need for mechanical ventilation during the 28 days following admission to the hospital and enrollment in the study. Secondary endpoints include things like transfer to the ICU, nuances of neurological, cardiovascular, thromboembolic, or renal disease, and death. The first hundred patients randomized into the study will inform a go-no-go decision by the data safety monitoring board. If the DSMB recommends the trial continue, the remaining 266 patients will be enrolled. We hope to reach that go-no-go decision by the end of the second quarter. Turning now to INKmune, our NK cell priming platform. NK cells are cells of the innate immune system that play a crucial role in cancer outcomes given their ability to target residual disease, the cause of cancer relapse. NL restores the function of the patient's own NK cells to attack their residual disease. We believe that by eliminating residual disease, INKmune should improve survival in cancer patients. This year, we plan to initiate a single-center phase 1 trial in high-risk MDS patients—that's Myelodysplastic syndromes, a precursor to acute myeloid leukemia that primarily affects elderly patients. This trial is set to run in the UK. The UK, like the rest of the world, where we would do clinical development, has had restrictions on the startup of new clinical studies because of the strains of the pandemic on their healthcare system. We are ready to enroll patients, and when the National Health Service gives us the green light, we will initiate the trial that will include at least nine patients with the opportunity to expand both the number of centers and the number of patients. Finally, we have previously announced that INB03, our oncology program, has been delayed due to COVID-19. We hope to initiate a phase 2 trial in MUC4 positive cancer once the pandemic is controlled. Although this program is clinically dormant, laboratory research on the combination of INB03 with tyrosine kinase inhibitors and MUC4-expressing tumors continues. Similarly, our eliminate program for NASH will not begin a phase 2 until the pandemic is completely controlled. We hope to have more clarity on these programs once we have reached herd immunity in the U.S. and the danger of these viral variants is understood. I will now turn it back to David Moss, INmune Bio's CFO, to discuss the financial results and upcoming announcements.

Thank you, RJ. I will provide a brief overview of our financial results and upcoming milestones. Net loss attributable to common stockholders for the year ended December 31, 2020, was approximately $12.1 million compared to approximately $7.7 million for the year ended December 31, 2019. Research and development expenses totaled approximately $5.9 million for the year ended December 31, 2020 and compared with approximately $3.3 million for the year ended December 31, 2019. The primary reason for the increase in expenses was an increase in R&D activities related to our clinical programs and costs associated with manufacturing additional drug supply. General administrative expense was approximately $6.3 million for the year ended December 31, 2020, compared to $6 million for the year ended December 31, 2019. At December 31, 2020, the company had cash and cash equivalents of approximately $22 million with no debt. Subsequent to the end of the quarter, we raised gross proceeds of approximately $28.4 million through our at-the-market or ATM facility and issued 1,439,480 shares of common stock at a price of $20.17. Based on our current operating plan, we believe our cash is sufficient to fund our operations and achieve potentially value-creating milestones into late 2022. As of March 4, 2021, the company had approximately 14.9 million shares of common stock outstanding. Now I’d like to move on and list our upcoming milestones and catalysts. This current year, we plan to initiate a phase 2 trial of XPro1595 in treatment-resistant depression, that is partially funded by a $2.9 million NIH grant. We also plan to report additional data on our phase 1b Alzheimer's disease program prior to the phase 2 program initiating. Additionally, towards the end of the year, we plan to initiate a phase 2 program for Alzheimer's disease with XPro1595 in patients with neuroinflammation. We will provide more clarity on the design of this program, including the cost of the phase 2 trial, as we get closer to this milestone. In addition, assuming the clinical landscape has not changed, we are planning trials in our other programs once the COVID-19 pandemic has been controlled and our trial sites give us the go-ahead. These include the INKmune phase 1 program for high-risk MDS and ovarian cancer, LIVNate phase 2 program for the treatment of NASH, and INB03 phase 2 for the treatment of MUC4 resistant metastatic Her2-positive breast cancer. So, in summary, notwithstanding the pandemic, we believe we are making good progress particularly in our neuroinflammation franchise following the compelling expanded Alzheimer's disease data that we reported in January. At this point, I’d like to thank you for your time and attention, and I’d like to turn it back to the operator for Q&A. Rob, could you please poll for questions?

Thank you. At this time, we'll be conducting a question and answer session. Our first question comes from Tom Shrader with BTIG. Please proceed with your question.

Good afternoon. Thanks for the update. Just the phase 1b trial, will we see more patients or will this be deeper analyses and patients followed for more time?

Yes. Thanks, Tom. You're going to see both. I think I have made it clear that we are exploring additional doses and so we will have more patients, and we will also have the patients that have been studied for a longer time. So you're going to get both; more doses and longer time.

Okay and then I hope this isn't too big a question, but for TRD, how do we think about this? Is this a subset of patients with systemic inflammation? Is this all patients, and just a little bit of a sense of is there any hints as to the time course of helping these patients and if they have TRD from inflammation are they reversible or would this be a stabilization? I know that's like 80 questions.

So, I'm going to give you the way we think about it. We clearly think that it's a subset of patients with treatment-resistant disease. If you look at the biomarkers we used, we think about a third of those TRD patients probably have biomarkers of inflammation. That's the group we're going to focus on initially. Remember, we do our CNS trials kind of like an oncology trial; we look for those biomarkers. It's not to say that those other patients wouldn't benefit, but at this time we don't have any data to support that. So in those patients that have biomarkers of inflammation, the data we have suggests you will see a response in three months, basically probably actually shorter, but the trials are designed to last three months because that's what the initial data shows. Now, I think the more interesting million-dollar question is, do these patients then remain on XPro, or does this reset them so they now become responsive to, let's say, an SRI or something like that? We don't know the answer to that. We do know that when patients are enrolled, we will not be taking them off their current therapy. So they will end up on double therapy or combination therapy, and then it will be up to their clinician to decide at the end of the study, just like we do in Alzheimer's whether we'll be keeping them on XPro as kind of a compassionate use or if it will actually be stopped. But I think that that's the second question that we need to answer. The first question is our hypothesis is clear that patients with treatment-resistant disease who have biomarkers of inflammation will respond to therapy if you get rid of that neuroinflammation, and that's what XPro is all about.

Got it. All right. Thank you. That's very helpful.

Our next question comes from Jonathan Aschoff with ROTH Capital Partners. Please proceed with your question.

Thank you. Guys, I was wondering if you were looking at any different neuroinflammation biomarkers for TRD versus what you're doing now for AD.

Yes. Thanks. Well, as we mentioned, there is this very special connectivity biomarker that you can see using functional MRI in the TRD patients. So that is a unique biomarker to that patient population. We will be measuring all of our standard MRI biomarkers, as we're interested in both white and grey matter markers of both inflammation and quality such as cortical disarray measurements. We will be measuring them also, but those are secondary exploratory endpoints. For the most part, what's driving the TRD program will be really standard clinical measures using validated clinical scales of depression and really anhedonia, but also this very unique observation using fMRI of connectivity that's associated with symptoms in these patients.

Okay. Thanks. Last question is I was wondering to what extent have you had inbound interest from investigators wanting to use your anti-TNF indications for which you are not planning trials?

So we have a significant effort that is at the preclinical stage. In other words, people ask us all the time, can I get the drug to study this model of neurodegeneration with that model? We have a very extensive and carefully curated program that we then harvest the best of the best of these data, and I can tell you there is a number of programs that you have not heard about yet that we have not announced that are very promising. For now, on the clinical front, our focus is really on the programs we've announced. We believe that the CNS franchise in neuroinflammation is making progress in Alzheimer's disease and we think that will bring significant value creation that will then allow us to expand into some of these other really unmet needs that we have on tap.

Our next question comes from Swayampakula Ramakanth with H. C. Wainwright. Please proceed with your question.

Thank you. This is RK from H. C. Wainwright. Couple of quick questions. On the Alzheimer's disease program, what additional data should we expect from the phase 1b, and also you're talking about initiating a phase 2 program in neuroinflammation in AD patients. What sort of timeframe are you thinking of?

Yes. Thanks, RK. So we are, as I've mentioned publicly, we're exploring doses in between the current cohorts of 0.3 and 1 milligram per kilogram. We see there is a dose response between those two groups as it relates to both measuring white matter free water and also looking at the CSF proteome. So I'm not convinced we have nailed the dose so to speak. So we're exploring that. The reason that we're spending time, even though there is no safety signal, there is no reason that we can't use the one milligram per kilogram per week dose; the average Alzheimer's patient survives seven years without therapy. We expect patients who have therapy to have extended survival. So we can see that a patient will be on drug for, let's say, 10 years, and so we want to nail the dose because that makes a difference, and once you do a registration trial, it's very hard to change the dose. So we want to have the right dose going into phase 2. So that is one of the primary bits of information you will get in mid-year when we kind of do our final download on the phase 1 trial as it relates to how we're going to do the phase 2. The second issue is what I call the duration issue. I mean currently, if you look at any of the amyloid studies, both what Biogen and Lilly have done, they're both 18-month studies. To me, 18 months in drug development—to do an 18-month study is a minimum of two years, probably closer to three years, and I'm getting old fast. I don't want to have to wait three years to do a phase 2 study and then another three years to do a phase 3 study. We think that with all of the sophisticated biomarker analytics that we have in place, we can shorten a trial. In other words, we don't think it has to be 18 months. I don't know whether we can cut it in half or not yet, but that is the second question we plan to answer in the next few months before we really publicize the design of the phase 2. So dose, duration, and the third thing is design, which is just kind of fine-tuning the cognitive endpoints so we make sure we have the right one because our goal once we launch the phase 2 trial is that it's going to be a trial that hopefully not only enrolls quickly but is short enough so we can maybe we can do a nine-month trial and then a registration trial in nine months, and basically we get to the market in the same amount of time that it takes for a more traditional amyloid 18-month trial to do their registration trial, i.e. the Lilly situation. So that's what you can expect in the next few months. As I mentioned with Tom Shrader, not only are you going to see data on more patients, but you're going to see the 3Ds: dose, duration, and design, and when we talk to you mid-year, we are going to be very explicit about those elements and be very explicit about what the phase 2 trial looks like. We expect to treat our first patients in the fourth quarter. I don't want to give you a date or time yet, but we're pretty comfortable with that plan.

Thank you. Thank you for taking my question.

Our next question comes from Daniel Carlson with Tailwinds Research. Please proceed with your question.

Hi guys. Thanks for taking my questions. Two questions. First off, with regards to Quellor, we know that you reduce neuroinflammation. Wondering if you think this will have any impact on long COVID.

Well, I've been waiting for that question, Dan. Thank you. So we have been very interested since day one when the early symptoms of losing your sense of smell and taste were identified. We've been looking for a strong signal that there is a neuroinflammatory component, quite frankly, and I'm so I'm talking about we've been looking at this for a year, and as some of the prime other than shortness of breath, the primary symptoms of long COVID would appear to be neurologic. They are brain fog, they are fatigue, they are depression, and there are plus or minus sleep disorders. Those look like CNS symptoms, but until literally two or three weeks ago, there was not a convincing publication that neuroinflammation played a role here, and the last thing we wanted to do was launch on a quixotic clinical trial. So we continue to watch this very closely. You can imagine we're very interested, and I think that there will be more information coming down the pike on the role of neuroinflammation. If not, I don't even need a consensus—if there is a building bit of data that suggests neuroinflammation plays an important role in long COVID, you can bet we're going to have serious conversations about this because 10%, at least 10% of patients with COVID-19 infections end up with long COVID symptoms, and they can be quite debilitating. So 10% of the millions of patients is a very big opportunity, and if it is neuroinflammation, we might have the drug that should be tested in the disease. So all I can say Dan is you're right, but stay tuned; no decisions have been made yet.

Okay. That's great. Thank you. Next question: can you tell us how many patients have passed the 12-week period at this time, and importantly, in my mind, how many of them—and I guess the three in the lower doses are not still on a drug—but in the higher dose, how many of those are still on the drug at this point?

Yes. So the lower dose patients are not on the drug, and it took us a while to get the amendment in place for the continuation trial. They wanted to be on the trial, but we didn't have the regulatory elements in place. So of the six patients in the high dose group, everyone enrolled for the extension trial. So all patients are eligible for nine months additional therapy. Three of those patients have reached their one-year anniversary, and two of those three have applied for special access, so they will continue on the drug. In Australia, the way they have a system where you can—the physician and the patient and the company can petition the government to allow them to stay on drug. So currently, we will have two of the three that are beyond the year approved for the special access program, and the third one is in the process; we just haven't had approval yet on that. So I guess the way to look at it is they're quite— I mean, the patients and their physicians think the drug is working, or let me put it this way: the patients and their physicians feel that they want to stay on the drug, and we believe that's a positive sign.

I agree. Well, just want to say congrats on tapping your ATM. I think it was a great job, and thanks for that; you guys are doing a great job, so keep up the good work. Thank you.

Our next question comes from Brett Conrad with Longboard Capital. Please proceed with your question.

Hello, yes. Thanks. Actually, one of my questions got answered by Dan's question, but I have a second one too on the Quellor trial, and given that kind of current rate of enrollment, can you give us some general dates in terms of when we expect to get a data readout and if that's positive, how long it will take to kind of complete the whole thing with the additional, I guess, 166 patients?

So as I said in the presentation, we expect to reach the DSMB go-no-go mark for the first 100 by the end of the second quarter, and assuming we get the green light to go forward, we expect to complete that enrollment; I think end of year is reasonable unless the disease just disappears with the vaccinations, but that isn't going to happen. We're not that efficient, and there are going to be enough people who aren't vaccinated out there to keep the disease in the news, so to speak. So our first goal is to reach the go-no-go decision by the DSMB. I want to remind everyone that this is not really a data readout. The only thing they can do is say stop the trial because things aren't working or continue to enroll, which would be a sign that things are probably behaving appropriately, but we're not going to get any kind of data report that says 50 patients did that, this 22 patients did that, etc. That's just not the nature of the data readout as the trial is currently designed.

Got it. Okay. That makes sense because it's a double-blind; you only actually even know until it's all over; you guys won't even be able to look at those interim data points, sounds like.

No, exactly; and as you know, I wear two hats on both the CEO and the Chief Medical Officer, so I'm the medical monitor, the company medical monitor. There are external medical monitors as well. So I see all the reports of problems with the patients, but I can't tell anything about whether they've gotten the drug or not. I can guess, but this is not—I don't do that. I've been doing it long enough you don't make guesses. So the FDA is adamant, and we agree that these need to be blinded placebo-controlled trials, and that's what it is. It’s frustrating as hell, but it's the right way to get the right answer.

Are you guys seeing any changes in the FDA in terms of their urgency lately in terms of getting treatments for COVID? Do you see that changing as the disease diminishes, or do you think—what's your opinion, because I know they also come and go; the FDA does in terms of their decisions and emphasis?

So Janet Woodcock, whom I respect, is a very experienced—the new director of the FDA, and you can see some changes occurring in some areas. I've not had any sense of that in COVID-19, but that's a personal one company experience. But I mean, the FDA deserves a lot of credit for the way they've handled the pandemic, and Janet Woodcock is—I couldn’t be happier to have her leading the agency. She does what's right for patients, and if you take the approach that we do, that it's all about what happens at the bedside, I'm confident that the FDA will respond appropriately when we provide them good data.

Our next question comes from Michael Irwin with Univest Security. Please proceed with your question.

Hi, Michael Irwin from Univest. I have one question about Alzheimer's and depression. So there has been a recent study that indicates that depression or patients with depression are more likely to develop Alzheimer's disease by about one and a half years, and XPro is being tested for both Alzheimer’s disease and depression. So how do you see this affecting XPro1595?

Yes. Thank you. That's a pretty interesting question. Actually, the way I interpret that data shows how neuroinflammation cuts across all of these various diseases. So neuroinflammation contributes to both depression and Alzheimer's disease, and there are some people that get both. Actually, there are also a lot of patients with Alzheimer's disease that have depression as a symptom, and it's recognized as one of the symptoms, and I believe there's even a drug approved for treatment of depression and Alzheimer's disease. So there's no question that there is an intersection. The intersection, though, is related to a common pathology—that's neuroinflammation—and that's exactly what XPro1595 is targeting: neuroinflammation, and neuroinflammation—if you get rid of neuroinflammation, the animal data suggests good things happen in the brain, and our clinical data is beginning to support that when you get rid of neuroinflammation, positive things happen in the CNS.

At this time, we've reached the end of the question and answer session. I would now like to turn the call back over to RJ for closing comments.

So thank you. That concludes today's call. Thank you for joining us. We look forward to our next quarterly update, and all I can remind everyone is to please get vaccinated and wear your mask even after you're vaccinated, and we'll speak to you again in May.

This concludes today's conference. You may disconnect your lines at this time, and we thank you for your participation.