Greetings and welcome to the INmune Bio First Quarter 2021 Earnings Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. 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 Chief Financial Officer of INmune Bio. David, the floor is yours.

Thank you, Doug and good afternoon everyone. We thank you for joining us for the call of INmune Bio's first quarter 2021 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 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 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, with the forward-looking statements behind us, I'd like to turn the call over to Dr. RJ Tesi, Co-Founder and CEO of INmune Bio. RJ?

Thank you, David and thanks everyone for joining the call. I will arrange my remarks to highlight the key takeaways for the first quarter 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. As I did last quarter, I will begin today's call with XPro1595 which we are developing for Alzheimer's disease and other CNS indications where neuroinflammation plays an important role. Recapping our hypothesis, neuroinflammation results in synaptic loss and neurodegeneration also known as nerve cell loss or death in patients with Alzheimer's disease. Nerve cells are where the memories are stored. Synapses are the wires that allow the nerve cells to communicate. Cognitive decline can occur when nerve cells die that is the memories are lost or with synaptic dysfunction that is the nerve cells can't communicate with each other. The combination of synaptic dysfunction and neurodegeneration causes cognitive decline in patients with Alzheimer's disease. We believe that for a drug to be effective in treating Alzheimer's disease, it must fix one or both of these pathologies. Based on data released so far, XPro1595, the drug we are developing for the treatment of Alzheimer's disease appears to improve both pathologies. Our Alzheimer's program is all about targeting and controlling neuroinflammation with XPro1595. We believe neuroinflammation is a core pathology of Alzheimer's dementia that must be controlled to treat cognitive decline. On the 23rd of January, we reported data on nine patients who had completed the full 12-week treatment period with XPro, three in the low-dose group and six in the high-dose group of one milligram per kilogram once a week as a subcutaneous injection. We expanded the data presented from that we had presented in July of 2020 to provide additional insight into the effects of XPro1595 in these patients with Alzheimer's disease. I will focus on four highlights of that presentation. We demonstrated a highly significant correlation between measures of white matter free water using MRI with inflammatory cytokines in the CSF obtained by lumbar puncture. XPro caused both measures to decrease substantially and significantly suggesting that white matter free water may be a non-invasive measure of neuroinflammation that will spare patients the need for an invasive lumbar puncture to sample CSF. The CSF proteome data provides hints to the benefits of controlling neuroinflammation with XPro. Highly significant decreases in neurofilament one and Visinin-Like protein one both biomarkers of neurodegeneration suggests nerve cell death is decreased. Significant increase in synaptic proteins Contactin-2 and Neurogranin demonstrate improved synaptic function. We presented an example of CNS remodeling in a patient who over nine months of weekly XPro treatment had improvements in impaired fiber density, a novel measure of white matter quality, and improvements in cortical disarray measurements, a novel measure of gray matter quality. Although, we only showed one patient this result was not unique. Eight of the nine patients reported in January were stable or showed improved cognition over the three-month period and the patients who responded with the greatest decrease in neuroinflammation had the greatest improvements in measures of their cognitive performance during those three months. Of note, we presented the scans of white and gray matter quality in a patient in that presentation. This patient was unique because we had the scan, but he had to quit or retire from his work because his dementia was progressive. After six months of XPro therapy, he was able to return to work. We continue to follow these patients who are on the extension study and intend to provide further updates on their progress. I would encourage you to review the KOL webinar from the January 21 presentation. It is available on our website. Also, all of what I've talked about is available in slide format in our non-confidential corporate slide deck also found on our website. We find these results compelling. They clearly demonstrate that the treatment with XPro1595 when given as a once-a-week subcutaneous injection for at least three months in patients with neuroinflammation with Alzheimer's disease have a decrease in that neuroinflammation. We remain committed to starting a blinded randomized placebo-controlled study by the end of the year. In the meantime, we continue to generate data in our Phase I trial and in the patients who opted to stay on XPro in the extension study. As a reminder the duration of the Phase I study is three months. The patients can then opt to join an extension study that allows an additional nine months of therapy. We have a handful of patients who have been on XPro for a year. When we report additional data from the Phase 1 this summer, we will provide data from new patients in the three-month study, additional biomarker data in all patients give insight into those who receive long-term XPro therapy in the extension study and provide details of the Phase 2 trial design. Needless to say, based on our results to date, we are very excited about the future of this program. A remarkable attribute of XPro1595 is its ability to control neuroinflammation really cuts across a large range of neurodegenerative and psychiatric diseases where neuroinflammation is a core pathology. What do I mean by that? If you're developing a drug that targets amyloid, you can really only treat Alzheimer's disease. With XPro1595, we can treat any CNS disease where neuroinflammation plays an important role. So that gives us a much bigger operating field. A current example is to use XPro1595 for the treatment of treatment-resistant depression. This Phase 2 trial is supported by a $2.9 million grant from the Small Business Innovation Research administration associated with the NIH and we will receive that money over the length of the Phase 2 trial. The treatment-resistant depression market is substantial. In the US, an estimated seven million patients suffer from TRD. The current treatment paradigm involves a trial-and-error cycling through therapies to find one that works. A patient is labeled treatment resistant once they have failed two regimens. This hit-and-miss approach is frustrating for patients and the clinical team and increases the cost of care, and that cost is substantial. It is estimated that the cost of treatment-resistant depression exceeds $64 billion a year to the US health care system. There is a real need for therapeutic advancements. As with the Alzheimer's trial, we will use biomarkers of inflammation to confirm that treatment resistance is likely due to neuroinflammation. Once the diagnosis is confirmed, patients are enrolled treated for six weeks to determine response to XPro therapy. The use of biomarkers is not routine in psychiatric drug development. We believe a precision medicine approach will make development of new drugs for depression more efficient and will provide more effective therapies. We will conduct this trial in collaboration with two of the world's pioneers in the field through Andy Miller and Associate Professor Jen Felger both of Emory University. The six-week trial will be a double-blind placebo-controlled study of XPro versus placebo 45 patients per arm. Biomarkers of inflammation will be measured at baseline two and six weeks. The primary endpoint is improved functional connectivity measured by MRI and reduction in biomarkers of inflammation. Secondary endpoints include clinical measures of motivation, which is the most sensitive measure in patients with treatment-resistant depression. We are on track to begin this trial later this year. Quellor is the name of the drug we used to treat patients in our COVID-19 program that targets cytokine storm in patients hospitalized with respiratory compromise due to COVID-19. The double-blind, randomized, placebo-controlled trial is designed to enroll 366 high-risk COVID-19 patients in two equal-sized cohorts. One cohort is a placebo plus standard of care, while the other is Quellor plus standard of care. The primary endpoint is the need for mechanical ventilation or death during the 28 days following enrollment in the study. The secondary endpoints include transfer to the ICU new onset of neurologic, cardiovascular, thromboembolic or renal disease. This summer, the Data Safety Monitoring Board will give us a go, no-go decision after evaluating the data in the first group of patients. If a go is given, the trial will proceed and ultimately, 366 patients will be enrolled. INKmune is our NK cell priming platform. As you know, NK cells are part of the innate immune system, that play a crucial and increasingly important role in cancer outcomes. They have the ability to target both active disease and particularly target residual disease, which is the cause of cancer relapse. In fact, T cells play very little or no role in clearing residual disease that is the cause of relapse in patients with cancer. This has been a frustrating trial to get off the ground because of the many months of COVID-related delays across the UK, but we are screening patients for treatment in the Phase 1 trial of INKmune patients with high-risk myelodysplastic syndrome or high-risk MDS. High-risk MDS is a serious hematopoietic stem cell disorder, in which patients have functionally effective NK cells, and this allows their marrow to be overtaken with blasts, which prevents progression of the disease and ultimately decreases survival. Approximately one-third of the MDS cases progress to AML. Current treatments include chemotherapy and bone marrow or stem cell transplantation, but these patients are elderly. Many of them are not candidates for chemotherapy or aggressive transplantation strategies. So, immunotherapy makes sense. In this trial, we hope to show that by delivering a therapy that primes NK cells, that therapy is INKmune. The patient's own NK cells, and I emphasize their own NK cells can be reprogrammed to kill the tumor. This open-label study will enroll nine patients in the dose escalation strategy. All of these patients will have MDS with excess blasts. The primary endpoint is safety and tolerability of INKmune administered IV. Secondary endpoints include the change in the number and percentage of blasts. Overall response rate, which is really hematologic measures in these patients using the WHO criteria and the duration of that response. We have the opportunity to expand the trial. It can easily move into a Phase 2, if the results are attractive. We recently put a short five-minute video up on our website. That does a wonderful job of explaining why NK cells failed to clear cancer. INKmune provides the trigger needed to activate these cells to kill resistant tumors. Finally, as we indicated last quarter and there's been no change INB03 our promising 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 better controlled. Although this program is clinically dormant laboratory research on the combination of INB03 with tyrosine kinase inhibitors in MUC4 expressing tumors continue. Similarly, we have not initiated a Phase 2 trial in NASH and this will not occur until the pandemic has been completely controlled. We hope to have more clarity on these programs once the future of the pandemic is better understood. I will now turn the floor back to David Moss, our CFO to discuss the financial results and upcoming announcements.

Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones. Net loss attributable to common stockholders for the quarter ended March 31, 2021 was approximately $4.6 million compared to approximately $2.0 million for the comparable period in 2020. Research and development expenses totaled approximately $2.5 million for the quarter ended March 31, 2021 compared with approximately $800,000 for the comparable period in 2020. The primary reason for the increase in expense was an increase in R&D activities related to our clinical programs and costs associated with manufacturing additional drug supply. General and administrative expenses was approximately $2.1 million for the quarter ended March 31, 2021 compared to $1.3 million for the comparable period in 2020. At March 31, 2021, the company had cash and cash equivalents of approximately $45.3 million with no debt. The cash includes net proceeds of approximately $28.4 million that we raised through our ATM facility during the three months ending March 31, 2021. As of May 5, 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. As RJ had pointed out earlier, this summer we'll provide a go or no-go decision by the Data and Safety Monitoring Board following the first group of patients treated regarding the continuation of our Quellor trial for the treatment of pulmonary complications from COVID-19. Towards the end of this year, we plan to initiate our Phase 2 Alzheimer's disease program with XPro1595 in patients with neuroinflammation. We'll provide more clarity on the design of this program including the estimated cost and timeline of the Phase 2 trial as we get closer to this milestone. Also towards the end of the year, we plan to initiate a Phase 2 trial of XPro1595 in patients with treatment-resistant depression that is partially funded by a $2.9 million NIH grant that we should receive over the length of the Phase 2 trial. Furthermore, as RJ mentioned earlier we are currently screening patients for the INKmune study in high-risk MDS and will report further information as this trial moves forward. 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 a go ahead. These include LIVNate Phase 2 for the treatment of NASH; INB03 Phase 2 for the treatment of MUC4-resistant metastatic HER2-positive breast cancer. So in summary, notwithstanding the pandemic we believe we're making very good progress particularly in our neuroinflammatory franchise, following the compelling expanded Alzheimer's disease data that we reported in January. At this point, I'd like to thank you very much for your time and attention. And I'd like to turn it back to the operator, Doug to pull for questions.

Thank you. Ladies and gentlemen, at this time we would be conducting the question-and-answer session. Our first question comes from the line of Jonathan Aschoff with ROTH Capital Partners. Please proceed with your question.

Thank you. RJ, can you tell us what biomarker data we can expect to see in the final Phase 1 Alzheimer's data release, and if the FDA favors any specific markers?

Okay. Thank you Jonathan. Remember the purpose of that trial is really two-fold. One is to help us define which biomarkers to use for patient selection in our Phase 2 trial. And two to really use, shall we say indirect measures or provide indirect evidence of the biology of improvements in the brain. So when I talk about biomarkers, I'm talking about things like white matter free water, apparent fiber density, looking at CRP in the blood those are biomarkers of inflammation and of improvement of cortical tissue. The FDA quite frankly doesn't yet care about these. They have made it abundantly clear that the only approvable endpoints for Alzheimer's disease relate to improvements in cognition using some choice of a panel of analytics that are well-established in the literature. So to be blunt, the FDA doesn't care what biomarkers we want to use. They're going to be looking at those cognitive endpoints, which will be part of the endpoints in the Phase 2 trial. Our biomarkers help us pick the patients, pick the dose, pick the duration, design the study to hopefully prevent us from having a study that's not conclusive. So I just use this as think about a biomarker that is used for oncology. The biomarker can either be used to help with the drug development, patient selection, et cetera or be used as a validated surrogate biomarker for efficacy. Progression-free survival is a great example of a validated surrogate endpoint, although it doesn't predict overall survival of the FDA acceptance. To my knowledge there are no validated surrogate endpoints in Alzheimer's disease. So for our Phase 2 and beyond trials, we will always use cognition as an important endpoint because at the end of the day as it stands now that's the only thing you can get approved for with the FDA in Alzheimer's. Does that answer your question, Jonathan?

Absolutely. Thank you very much, RJ. That's all that I had.

Our next question comes from the line of Mayank Mamtani with B. Riley Securities. Please proceed with your question.

Hi. Good afternoon. Thanks for taking my question. And congrats on the progress. So in terms of just following up on the previous question on the upcoming extra data disclosure. RJ, could you clarify how many patients you may have on the low and high dose? And also on the free water update that biomarker, would you have more patients that you could report more data on that? And then I have a follow-up on the phase 2 study design.

Thank you, Mayank. We expect to have at least 17 patients, possibly up to 18 or 20, and even as many as 24 for the data analysis. It’s important to note we are looking at two categories of data, and I appreciate the opportunity to discuss this. As I mentioned, the primary trial lasts for three months, during which we will gather white matter free water data from all patients. Additionally, we will collect some of our more intriguing biomarkers, such as apparent fiber density and cortical disarray measures on these patients. Once patients transition into the extension trial, they will still receive biomarker data—though not from CSF, but from blood samples and MRI scans at six, nine, and twelve months. While it won't be a complete cohort, many patients reaching those time points will have scans, cognitive testing, and safety labs conducted. This will allow us to broaden the information we can provide, increasing both the number of patients and the duration of therapy. I want to emphasize that at the three-month mark, all patients will have had their CSF proteome analyzed. The CSF proteome offers a vast wealth of information, containing approximately 37,000 proteins, of which we've only reported a small fraction. We continue to explore this data, and it's quite compelling. From your perspective as investors, we will provide updates on a larger patient group, following them for up to a year. We will feed this data into our analysis, and in the August release, one of our key objectives will be to present clear guidance on what to expect from Phase 2, including details on the patient demographics, duration, and dosage, as we plan to initiate it shortly thereafter. As you know, the Phase 2 blinded placebo-controlled trial is a critical step for the success of this program.

Right. Thank you. That was very helpful. And then on the phase 2 design, RJ, are there any biomarkers here that, be it MRI, be it blood, any that you feel could have prognostic value where you could have an enrichment strategy for maybe identifying the early responders and maybe following that through in your longer-term kind of study? I'm just curious, since you are seeing some movement in these biomarkers at a very short time period.

So. Great question. And so as you know when we designed the trial really to focus on neuroinflammation. And we selected patients who had either an elevated CRP, elevated sed rate, elevated hemoglobin A1c, or were APOE4 positive. And based on our analytics to date we – to the credit of CJ Barnum who's the Head of our Neuroscience Program, I think we got it right. We did a good job selecting those patients, right, because those patients all had neuroinflammation by both CSF cytokines, which is what you're used to seeing, and by the white matter free water. So we're pretty comfortable with our patient selection. We have some of the – we are very intrigued with some biomarkers that may show evidence of early response. And we'll be talking more about that in August. We're not yet ready to go public, but I will say unequivocally that our biomarker strategy is paying dividends. Some of that is you just get lucky. When you're doing something novel like this, you have to make some informed guesses. Our informed guesses are turning out to be pretty good and we will provide all that data going forward. But just think about white matter free water as being a little bit of a tip of an iceberg here, because there's a lot – there'll be more interesting stuff coming behind. And I hate to leave you hanging, but you're going to have to wait till August.

Great. And just my final question was on – if anything like this any insight on the biomarker work you may also do in TRD, and if there's any read-through from the work you've done in Alzheimer's already?

Yes, that's a great question. The biomarker we are using is a functional MRI scan specifically designed for treatment-resistant depression. This work originated from Miller and Felger at Emory University. We plan to utilize all the strategies we've applied in our Alzheimer's trials for these patients as well. During our discussion, I mentioned that one of the advantages of XPro is its focus on neuroinflammation. Neuroinflammation affects a wide range of diseases in the central nervous system, including both neurodegenerative and psychiatric conditions. Therefore, the insights we gain from Alzheimer's can be applied to treatment-resistant depression, and vice versa. What we learn from these two conditions can also be beneficial for additional diseases. There's really no isolated case here, which is quite exciting. I cited the example of targeting amyloid with an anti-amyloid medication. Once you've addressed Alzheimer's disease with that drug, there aren't further applications for it. That's a favorable situation if you have an effective drug. However, in our case, we believe our approach will not only be effective for each specific disease but also that we can leverage this knowledge repeatedly across numerous conditions. You can refer to our website and publications to find a list of various diseases—around 10 or 12—that we aim to target with this single drug.

Great. Looking forward to updates. Thank you, RJ.

Our next question comes from the line of Jason McCarthy with Maxim Group. Please proceed with your question.

Hey guys. Thanks for taking the questions. Just kind of building a little bit more on the Alzheimer's disease. Given all the activity you've seen in the last, I don't know 12 months or so, around inflammatory biomarkers and use of biomarkers to advance to later stage trials, is the next Phase 2 program going to have call it 30 patients to 50 patients maybe a little bit more with a three-month biomarker endpoint that you could look at and say I have a drug here. We'll continue on with the cognition stuff out to 12 months, maybe six, nine, and 12 months. But we can start designing a Phase 3 around what we're seeing here. We did see it once before this year. And we're wondering if that's something that you're thinking about? Or how you're thinking about it?

Thank you for the question, Jason. I appreciate the challenge. I believe you are on the right track. We think the biomarkers will guide us in the right direction, but it's a bit too early to draw conclusions based on the data we have at three months and to predict what will happen in 12 months. The small number of patients we currently have limits our ability to make definitive statements. Once we have a larger patient group, we should be able to reach more conclusive results. There is historical evidence in Alzheimer's disease showing that three-month data can sometimes differ from longer-term findings, though this applies to a specific category of drugs. You're correct, and I've mentioned this before: we are making efforts to avoid an 18-month trial. Such trials may be necessary for anti-amyloid or anti-tau strategies since they take an indirect route to treatment. However, with XPro targeting neuroinflammation directly, we believe a shorter timeframe is sufficient. While I can’t provide a specific duration yet, I anticipate that our Phase 2 study will be significantly shorter than 18 months and will yield the necessary quality data. Our objective differs slightly from what you described. Our aim is to gather sufficient insights by the end of Phase 2 so that we can choose the right patient enrollment criteria for Phase 3, ensuring that we select patients likely to show positive results. So far, the straightforward biomarkers we used for enrollment have effectively identified patients with neuroinflammation, and with additional tools at our disposal, we expect to improve our targeting even further.

Got it. And on the treatment-resistant depression side, is the program going to have measures of depression along matter scores, pick your flavor or number of matter score? That's one question. And in terms of prioritizing mental health-related diseases like TRD, how do you look at it through the lens of what's coming down the road with all of the psychedelic-based companies piling into treatment-resistant depression because it's happening now and there's going to be a lot more NASDAQ listings in the next six to 12 months, and it's going to be right in the window of when you start this trial? Is that something that you're considering as well?

That's a good question. Yes, we are certainly measuring all the other aspects of depression. The lack of pleasure or motivation, which I referred to as motivation in the text, is the main clinical endpoint we are focusing on. This is a challenging treatment and a prevalent symptom in patients with treatment-resistant depression. The topic of psychedelics is intriguing. It raises the question of whether this is just a trend or something more substantial. I believe time will reveal the answer. I think it's fascinating how psychedelics are being repurposed to treat these difficult conditions. I feel confident about our ability to enroll the small number of patients needed for our trial at Emory and UAB, where the researchers are keen on understanding the role of TNF in this disease. If we find ourselves needing to conduct a larger trial with 500 patients afterwards, competition from psychedelics in drug development could pose challenges. For now, I will continue to monitor this situation with interest, just like everyone else.

That's right. My point was not about being distracted by trends on Wall Street. It's not about competing with them but rather about whether we will focus more on TRD as a public company due to these trends like NASH, which you are familiar with. That was my question as well.

Yes. We've been quite clear about our strategies. We prioritize the science over investor interest, with COVID-19 being an exception. During the challenging times of March 2020, we acted according to what we believed was right for the company. Generally, we adhere to scientific guidance and the funding we receive. For example, our engagement in Alzheimer's disease is due to a $1 million grant from the Alzheimer's Association, and our focus on Treatment-Resistant Depression (TRD) is supported by nearly $3 million from the NIH. While we may be opportunistic, we also have a drug that can be applied in various areas. However, we won't pursue new avenues without sound science backing them. Our scientific foundation is robust.

Our next question comes from the line of Thomas Shrader with BTIG. Please proceed with your question.

Hey, guys. This is Sung Nam calling in for Tom. First of all thank you for the update and taking my question. So kind of building off the biomarker for the XPro1595 for your ongoing phase 3 one trial for Alzheimer, I was wondering if we should expect any additional imaging biomarker data beyond the white matter free water for the future readouts.

Definitely. We are very excited about these developments. We've been collaborating with two vendors, Imeka and Oxford Brain Diagnostics. Imeka focuses on our white matter analytics, while Oxford Brain Diagnostics works with our gray matter group. We will have data on a larger number of patients and more extensive white matter free water data, which will provide increased breadth. Additionally, we are enhancing our understanding of white matter specifically, as there are biomarkers we only alluded to before, such as apparent fiber density, which has proven to be quite intriguing. However, we still need to conduct further work, and we are in close collaboration with Imeka on this, so you will hear more about it soon. The key takeaway is that CNS drug development is evolving. With the new tools at our disposal, we, meaning the biotech community, will improve our efforts in developing drugs in the CNS space. We, at INmune Bio, have been at the forefront of this progress and aim to demonstrate that to you every time we present new data.

Our next question comes from the line of Michael Irwin with Univest Securities. Please proceed with your question.

Hi. So there's recently been some research that shows the APOE4 gene has some link to Alzheimer's with brain inflammation causing damages synapsis and can also be used for early detection. Is it the gene of interest for research and development for XPro1595 moving forward?

So, yes. At this point, we used APOE4 which is a gene for one of our inclusion criteria. Interestingly, in the United States a lot of people know what their APOE4 status is. And as you know, it is enriched in patients with Alzheimer's disease. I don't think we are yet convinced of other gene approaches at this point. But I would say that we are always have an open mind. I mean, obviously, the beauty of genetic markers is they're relatively easy to get. But at this point, we do not have plans beyond APOE4. But as the data changes not only what's available to us but our own data changes, that may change.

Okay. And also there has been some research around a candidate drug sargramostim for the resurfacing for Alzheimer's drugs to create more white blood cells for fighting diseases and they have actually shown some promising data in a clinical trial. What is your opinion on the approaches in white blood cells? And can you elaborate on drug?

If I understand your question correctly, there are efforts to enhance white blood cell or macrophage activity as a potential treatment for Alzheimer's disease. While I can't comment specifically on those, I will state clearly that we agree with the idea that dysfunction in microglial cells, which are a type of white blood cell, contributes to Alzheimer's. These cells lose their ability to clear debris, especially amyloid debris, which is a fundamental issue. We believe that improving their ability to remove waste will help clean up the brain, leading to better outcomes in treating diseases. It's interesting to note, as Jason mentioned, that many new therapeutic strategies have emerged recently. A few years ago, we were practically alone in the Alzheimer's field aside from Biogen. This situation has changed, reflecting a growing optimism in the biopharma and investor community regarding potential breakthroughs in Alzheimer's, especially if the FDA approves aducanumab from Biogen this June. We are enthusiastic about this progress and welcome anyone who wants to join us on this journey. However, it's important to recognize that this is a challenging disease to address, but we are committed to finding a solution.

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

Hey guys. RJ a question for you about neuroinflammation as it relates to COVID. And I'm wondering if you guys are going to be doing anything in this anytime soon?

We're cautious about discussing our strategic plans until we're fully prepared to share them. However, we have been closely monitoring the long COVID situation. It seems to be a significant issue, and there are not many hypotheses regarding its causes. We believe neuroinflammation may play a crucial role, although the data supporting this is limited. The symptoms resemble those of neuroinflammation, but there has been little clinical correlation so far. We are closely observing developments in this area, and once we gather sufficient data and potentially attract funding from the government or NIH, this could become a viable option for XPro, provided we, along with the NIH and other stakeholders, are convinced of the importance of neuroinflammation.

Got you. And then if I could just ask one other question. Since it looks like if you're successful you'll be treating Alzheimer's patients for a very long time, I'm just wondering if you have any additional long-term safety data as XPro continued to be safe for your patients who are on it for 12, 18 months. And then also along those lines are you looking at any other delivery methodologies besides injection?

Yes, we do have some patients who have been on the drug for up to 12 months, and they continue to stay on it without any safety concerns leading to discontinuation after three months. It’s worth noting that existing TNF inhibitors are typically used for many years, and since this is an improved version, we believe the safety risks in this development program are lower compared to certain other drug types. We are exploring interesting delivery strategies for different diseases, which can enhance the drug's applicability. Additionally, we want to make administration easier for patients. Currently, patients have been quite comfortable with a weekly subcutaneous injection, which is not as frequent as injections required for diabetes. Our goal is to develop a convenient self-injector, similar to an EpiPen, that is well-tolerated. However, our primary focus right now is ensuring the Phase 2 trial design is optimal. If the Phase 2 trial does not meet our expectations, having different formulations and delivery systems won't be helpful. Well, thank you all for quite a long call. This was almost 90 minutes, and I appreciate you allowing me to stand on my soapbox, but part of that is because I think we are very excited about the XPro program in Alzheimer's disease. I think you can sense that from the way we present the data. And I think you should be able to sense an increasing confidence in our program as we go forward. And a lot of that is due to the credit of the team led by CJ Barnum. Likewise, the COVID and INKmune programs are coming along. We believe our future is bright. We thank you for your interest, and I can't wait until we get to see you all face-to-face again. Thank you very much.

Ladies and gentlemen, this does conclude today's teleconference. Thank you for your participation. You may disconnect your lines at this time. And have a wonderful day.