INmune Bio Inc. (NASDAQ: INMB), a biotechnology company specializing in the development of novel immunotherapies, reported promising developments in its second quarter 2024 earnings call. The company highlighted progress in its INKmune memory-like natural killer cell oncology platform and its ongoing Phase II Alzheimer's study. INmune Bio completed an interim analysis of its Phase II trial of XPro in early Alzheimer's disease, showing encouraging results, and is on track to fully enroll the trial by September's end. Additionally, the company raised approximately $14.5 million in gross proceeds from equity offerings and has sufficient cash to fund operations until 2025.
Key Takeaways
- INmune Bio's Phase II Alzheimer's trial interim analysis shows promising results.
- The company is set to complete enrollment for the Alzheimer's trial by the end of September.
- INmune Bio published a paper on the unique characteristics of memory-like natural killer cells generated by INKmune.
- Patient-level data from the Phase I/II trial in castrate-resistant metastatic prostate cancer is expected later this year.
- INKmune has demonstrated safety with no significant adverse events in clinical trials.
- The company has raised $14.5 million in gross proceeds from two equity offerings.
- INmune Bio has sufficient cash to fund operations until 2025.
Company Outlook
- The company plans to release top-line data from the Phase II XPro trial for Alzheimer's disease approximately six months after completing enrollment.
- A Phase II trial for treatment-resistant depression is set to begin in the second half of 2024.
Bearish Highlights
- The company did not report any negative updates during the earnings call.
Bullish Highlights
- INKmune has shown promising results in a research study and in clinical trials.
- The development program for INKmune has made progress with a new formulation and increased manufacturing capacity.
- INmune Bio sees opportunities for XPro in Alzheimer's disease and INKmune in castrate-resistant prostate cancer, with potential for applications beyond current indications.
Misses
- There were no specific misses mentioned in the earnings call.
Q&A Highlights
- Mark Lowdell and Raymond Tesi discussed the unique advantages of INKmune, including its cost-effectiveness and ease of shipping.
- The company detailed the enrichment process for patient enrollment in the Phase II Alzheimer's trial, focusing on patients with specific biomarkers.
- Christopher Barnum expressed confidence in the quality of the data collected from the Alzheimer's trial and the potential of XPro and INKmune.
INmune Bio's second quarter 2024 earnings call presented a positive outlook for the company's ongoing clinical programs. With advancements in its INKmune platform and Alzheimer's study, as well as secure funding to sustain operations for the near future, INmune Bio continues to make strides in the development of innovative treatments for challenging diseases. The company's focus on delivering data readouts swiftly demonstrates its commitment to progressing its clinical trials and bringing new therapies to market.
InvestingPro Insights
As INmune Bio Inc. (NASDAQ: INMB) forges ahead with its clinical programs and secures funding for its operations, a closer look at the company's financial health and stock performance reveals some challenges. INmune Bio's market capitalization stands at $163.4 million, reflecting the market's current valuation of the company.
InvestingPro Tips indicate that while INmune Bio holds more cash than debt, which is a positive sign for its financial stability, the company's stock has recently experienced significant volatility, with a notable decline over the past week. This could be a point of concern for investors looking for stability in their investments. Additionally, analysts are not optimistic about the company's profitability in the near term, expecting both a sales decline and a drop in net income for the current year.
The InvestingPro Data provides further insight into the company's financial metrics. INmune Bio is trading at a high Price / Book multiple of 5.81, which suggests the stock might be overvalued compared to the company's book value. This is further supported by the company's negative P/E Ratio of -3.97, indicating that investors are paying more for each dollar of loss the company incurs. Moreover, the company has experienced a significant revenue decline of 47.39% over the last twelve months as of Q1 2024.
In terms of stock performance, INmune Bio's price has been quite volatile, with a one-week total return of -7.81%, highlighting the risks associated with investing in the stock. For those interested in further analysis and metrics, there are additional InvestingPro Tips available at https://www.investing.com/pro/INMB, which can provide deeper insights into INmune Bio's financial and stock performance.
Investors considering INmune Bio as part of their portfolio should weigh these financial metrics and analyst expectations against the company's promising clinical developments. Balancing the potential long-term gains from successful trials with the current financial realities will be key in making an informed investment decision.
Full transcript - INmune Bio (INMB) Q2 2024:
Operator: Greetings, and welcome to the INmune Bio Second Quarter 2024 Earnings Call. At this time, all participants are in a listen-only mode. Later, you will have the opportunity to ask questions during the question-and-answer session. [Operator Instructions] As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it's my pleasure to introduce Mr. David Moss, CFO of INmune Bio. David?
David Moss: Thank you, operator, and good afternoon, everyone. We thank you for joining us for the call for INmune Bio's second quarter 2024 financial results. With me on the call today are Dr. RJ Tesi, CEO and Co-Founder of INmune Bio; and Dr. Mark Lowdell, Chief Scientific Officer and Co-Founder of INmune Bio, who will provide an update on INKmune, our memory-like natural killer cell oncology platform. Also on the call is Dr. CJ Barnum, Head of Neuroscience, who will provide some details on our ongoing Phase II Alzheimer's study. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those such as forward-looking statements. Please see the forward-looking statements disclaimers 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 forward-looking statements, which speak only as to 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 obligation to update these forward-looking statements to reflect future information, events or circumstances. With that behind us, now it's my pleasure to turn the call over to Dr. RJ Tesi. RJ?
Raymond Tesi: Thank you, David, and good afternoon to everyone. We will keep our prepared remarks brief. I will review the key takeaways from the second quarter, relevant news from recent weeks and provide updates on our platform programs. I will then pass it to CJ Barnum, VP of CNS Drug Development, for more details on the ongoing Phase II trial in Alzheimer's disease. Dr. Mark Lowdell will follow with an update on our INKmune program in prostate cancer, and David Moss will conclude with a review of our financial results for the second quarter before we take your questions. Since our first quarter conference call in May, we continue to make steady progress in both clinical programs. Before I comment on our AD -- on our XPro program in AD or in Alzheimer's disease, I want to make a couple of comments about the rapidly changing landscape of Alzheimer's disease, diagnosis and treatment. Just in the last month, a second drug, donanemab, was approved for the treatment of Alzheimer's disease. It is an anti-amyloid drug. And it does have a black box warning for highlighting the increased risk of area, which is edema in the brain in patients with two copies of ApoE4 gene. Last week, the EU regulatory authorities did not approve the Eisai-Biogen's drug lecanemab for the treatment of Alzheimer's disease. We don't know if the EU's decision is going to be unique to lecanemab or affect other drugs in the anti-amyloid class. Today, the last day of AAIC in Philadelphia, AAIC is the Alzheimer's Disease International Conference, which is the largest meeting in AD that occurs every year. But at this meeting, there is cautious hope for the future of therapeutic options for patients with Alzheimer's disease and a lot of discussion about alternatives to amyloid therapy. People understand the risk and efficacy profile of this class of drugs, and they look forward to other options in the future. Much excitement was focused on the anti-inflammatory treatment strategies. And obviously, we like to think we are leaders in this particular area. All in all, it was a very bullish meeting for XPro in Alzheimer's disease. In June, we completed a planned blinded interim analysis of AD02, our Phase II trial of XPro in patients with neuro early Alzheimer's disease with biomarkers of inflammation. The purpose of the analysis was to evaluate power and performance characteristics of the primary endpoint. The primary endpoint is EMACC, which is Early Mild Alzheimer's Cognitive Composite score. Independent third-party statisticians and neuropsychologists determined the AD02 trial as appropriately powered and concluded the trial design, operational execution, data collection and management are of the highest quality. As of today, we have many patients in the screening process and pipeline, and are on track to reach full enrollment of this trial by the end of September. We really await top line data readout on the primary endpoint approximately six months later -- or excuse me, approximately six months after the last patient is enrolled. At AAIC this week, we presented additional data on the effects of XPro in the brain of patients with Alzheimer's disease. The data demonstrate XPro's direct impact on synaptic proteins and provide biologic support for the improvement in synaptic function that we recently demonstrated with EEG. I remind you that synapses are the things that allow nerve cells to talk to each other, and they are a critical part of neurologic disease in general and Alzheimer's disease specifically. These data are another example of how XPro normalizes the brain's immune system to prove the biology of the aging brain that includes less neurodegeneration, that's nerve cell death, increased remyelination and improved synaptic function. We predict the ongoing Phase II trial will demonstrate these biologic benefits correlate with cognitive benefits. The importance of controlling neuroinflammation extends well beyond Alzheimer's disease, and we continue to move forward with our plans to initiate a treatment-resistant depression Phase II study. The trial is sponsored by the NIH, and we expect to enroll patients later this year. INKmune, our novel NK-focused cancer program, also continues to make progress. We announced the publication of a paper in the prestigious high-impact journal of ImmunoTherapy of Cancer. The data shows the unique ability of INKmune to create cancer killing memory-like NK cells in in situ, in situ meaning within the patient's blood system of using NK cells of their own. Dr. Lowdell will provide more detail on this in a moment. We're excited by these data and their implications for treating multiple types of solid tumors with INKmune in the future. We plan to provide patient-level data from the ongoing Phase I/II trial in castrate resistant metastatic prostate cancer later this year. For now, I'll turn it over to CJ Barnum, VP of CNS Drug Development, to provide more -- a more in-depth discussion of our ongoing Phase II trial in patients with Alzheimer's disease. CJ?
Christopher Barnum: Thank you, RJ. As you said, I'd like to take some time to discuss the ongoing Phase II trial in Alzheimer's and the recent unblinded analysis we performed. The clinical trial is powered on the Clinical Dementia Rating Scale or CDR, and is using both EMACC and CDR as our primary and key secondary endpoints, respectively. These clinically valid endpoints were chosen based on their ability to accurately assess cognition in our target population of early Alzheimer's patients with biomarkers of inflammation. It's our belief that patients on XPro for the treatment of early AD will have stable or possibly improved cognition, and our endpoints were selected to give us the best chance of a successful outcome. As RJ said, we are close to completing enrollment. This has admittedly taken slightly longer than originally forecast, and I think it's important to address why that is the case as it plays right into why we believe we'll get a positive result. At INmune, we are running the first clinical trial in Alzheimer's using biomarkers as selection criteria. Our trial is designed to have a small enrollment and a very short duration. Smaller studies require higher quality data to minimize the impact of variance. As such, patient selection is key to success. We need to enroll patients who are not only likely to benefit from our therapy, but are also highly likely to complete the duration of the trial. This selectivity leads to a slower enrollment process. We could easily relax our criteria to speed enrollment. However, there is a trade-off between speed and quality. We are very biased towards the latter. This focus on execution is demonstrated through the recently completed blinded interim analysis of our data. As that independent evaluation revealed and I quote, "The assumptions made during the planning are being met within the conduct of the trial." In other words, the EMACC is performing exactly as expected. This is a testament to our operational and clinical teams who continue to exceed my expectations in executing a trial of the highest quality. While the final results from the trial have yet to be determined, I can say with great confidence that the trial is being conducted in such a way that at completion, we will know without a doubt if we have a successful therapy. With that, I'll turn the microphone over to Mark to discuss the INKmune program, and I look forward to answering questions investigators might have about the Alzheimer's program. Mark?
Mark Lowdell: Thanks, CJ, and good afternoon, everybody, and thank you for joining us. As INmune announced recently, together with several of my colleagues, I was pleased to leave the publication of a landmark paper entitled proteomic and phenotypic characteristics of memory-like natural killer cells for cancer immunotherapy, which as RJ said, was published in the Journal for the ImmunoTherapy of Cancer. So in this study, we demonstrated that memory-like natural killer cells or mlNK cells generated by INKmune are the same as the more traditional cytokine-driven mlNK cells. And both type of NK cells show increased cytotoxicity against multiple tumor types. However, while most studies are conducted on NK cells from healthy volunteers, this study demonstrated that NK cells from cancer patients can be primed with INKmune and are equally as potent as those generated from healthy volunteers, providing further support for our in vivo treatment strategy. This research also provides new insights into the metabolic and proteomic mechanisms underlying NK cell memory, paving the way for innovative treatments in both hematological malignancies and more importantly, for us, multiple solid tumors. But this is an area of NK cell biology research that is evolving very rapidly, and our study is the first to identify the unique characteristics of mlNK cells. Most significantly, the study is the first to report in vivo generation of mlNK cells, as RJ said, and that's something which cannot be done with the cytokine cocktail used in vitro by other groups because of the toxicity of the cytokines. So our research successfully showed that these mlNK cells primed by INKmune can be found in patients' blood after they've been treated with the drug, which is a critical step in proving our claimed mechanism of action. We also believe this points ways to enhance the potential of mlNK cells in further advances in cancer immunotherapy. Our paper highlighted the improved metabolic function of mlNK cells, which predicts better performance in the tumor microenvironment or TME. We believe these findings are particularly noteworthy as NK cell dysfunction in the TME has been reported by many others to be due to impaired metabolic function. So showing that INKmune priming can overcome these metabolic barriers encourages our belief that INKmune will target solid tumors. And this is further supported by our observation in the same paper that INKmune priming increases survival proteins for nutrient receptors expressed on NK cells. And this combination of changes following INKmune priming is exciting for our ongoing clinical trial in metastatic castration-resistant prostate cancer. This research study was a commercial and academic collaboration led by INmune over many years, and we were delighted to see the results of the work published in a high-impact peer-reviewed scientific journal. Elsewhere in our INKmune development program, we're pleased to announce a new formulation of INKmune that supports the highest trial dose with a single bag administration, which makes it much more easily delivered in the clinic, and the expansion of our bioreactor capacity in preparation for more scalable manufacturing. So an IND amendment to the FDA with the improved formulation has been submitted. It also includes additional validation data supporting an alternative critical reagent used in the manufacture of INKmune to improve our supply chain redundancy. And all of these seem minor, but there are essential steps in preparation for commercial development and supply of the drug. Since our last call, we've completed the first cohort in our Phase I, Phase II open-label trial of INKmune in metastatic castrate resistant prostate cancer called CarePC. Following review by the Safety Review Committee, approval was granted to proceed with the second dose level, cohort 2, and we're nearly halfway through that cohort with patients in line waiting to be recruited. Data from this open-label trial are expected to be released intermittently as they become available for us. But most importantly at the moment, the safety record of INKmune remains excellent. There have been 12 administrations of INKmune in the CarePC study given as an outpatient with no significant adverse events and 0 cases of cytokine release syndrome. And combining those data with the experience from INKmune from the MDS/AML trial, over 25 infusions of INKmune have now been given safely without the need for conditioning therapy, premedication or cytokine support. So that ends my update on the INKmune platform, and I'd like to turn the call over to David Moss, our CFO, to discuss financials. David?
David Moss: Thank you, Mark. As usual, I'll provide a brief overview of our financial results and upcoming milestones before we head to our Q&A session. During our second quarter, we were pleased to have raised approximately $14.5 million in gross proceeds from two separate equity offerings over the past weeks at an average price of $8.35 to $9.84 per share. In the two transactions, the company issued an aggregate of approximately 1.558 million shares of common stock and warrants to purchase an aggregate of approximately 1.558 million shares of common stock. The warrants have a two year term with acceleration on positive Phase II data from our AD program, which if exercised would raise additional cash for the company. In the first approximate $4.8 million raise, management, employees and members of the Board of Directors purchased over $1 million of stock. I cannot underscore how financially committed and aligned the entire INmune team is to the success of the company. We greatly appreciate the support we saw in both offerings from mostly existing investors and our team here at INmune Bio, but we also welcome a few notable holders to the registry, including a sole investor in the approximately $9.7 million offering, a person that I've had a relationship with for more than a decade. In addition, we received approximately $2.5 million in R&D rebates in July as we continue to manage our shareholder resources carefully while completing our clinical programs. Now moving on to financials. Net loss attributable to common stockholders for the quarter ended June 30, 2024 was approximately $9.7 million compared with approximately $6.5 million for the comparable period in 2023. Research and development expense totaled $7.1 million for the quarter ended June 30, 2024 compared with approximately $4.1 million for the comparable period in '23. General and administrative expenses were approximately $2.8 million for the quarter ended June 30, 2024 was approximately -- compared with approximately $2.3 million for the comparable period in 2023. As of June 30, 2024, the company had cash and cash equivalents of approximately $31.1 million. Based on our current operating plan, we believe our cash is sufficient to fund our operations into 2025. As of August 1, the company had approximately 19.8 million shares of common stock outstanding. Effective as of July 1, the company joined the Russell 3000 Index as part of its 2024 reconstitution, a positive development for our company and our shareholders that we believe will increase our visibility within the investment community and help broaden our shareholder base. This is the first significant index the company has joined since going public in 2019. We also believe our inclusion in the Russell 3000 is a testament to the hard work and dedication of our entire team and underscores our commitment to advancing our innovative immunology and inflammation platforms in early Alzheimer's treatment -- in early Alzheimer's treatment-resistant depression and metastatic castration-resistant prostate cancer. Now I'd like to focus on some key upcoming milestones. As RJ and CJ have mentioned, we expect full enrollment in our Phase II XPro trial for the treatment of neuroinflammation as a cause of Alzheimer's disease before the end of Q3, and top line data is expected to read out approximately six months from the last patient enrolled. We will initiate a Phase II trial of XPro in patients with treatment-resistant depression in the second half of 2024. We expect to complete enrollment in the second cohort in the metastatic castration-resistant prostate cancer by the end of Q3 '24 and complete the Phase I portion -- is expected to complete enrollment by Q2 of 2025. Results of the trial be released as they become available starting later this year. Although we have secured additional funding, as always, we continue to focus on achieving our primary clinical objectives while remaining cost prudent with the potential to recover a portion of R&D expenses in Australia and the U.K. In summary, we secured a meaningful equity infusion that puts us in a good position into 2025 with our focus on remaining on execution. At this point, I'd like to turn the microphone back to RJ to conclude our prepared remarks and then go to Q&A. RJ?
Raymond Tesi: Yes. Thank you, David. This is an exciting time for the company. The therapeutic landscape of Alzheimer's disease is changing rapidly. And the changes are making the XPro program in Alzheimer's disease more -- I guess, the right word is relevant. As people get frustrated with the anti-amyloid strategies, they look towards neuroinflammation as a potential way to improve patients' lives. We expect to be reporting meaningful data from both the XPro and INKmune programs in what now seems to be the near future. Each of our programs has a strong scientific foundation. Our clinical trials are designed to take advantage of the unique biology each drug brings to patients. The company has funding to see the development through important milestones, and we are grateful for the strong and committed shareholder base that continues to support INmune Bio. And in particular, we thank those who are invested alongside us and management as we work to achieve our goals. So now I'd like the operator to poll for questions.
Operator: [Operator Instructions] And we'll take our first question from Tom Shrader with BTIG. Please go ahead. Your line is open.
Tom Shrader: Good afternoon. Thanks for taking the questions. Congratulations on all the progress. I wanted to ask a kind of a remedial question first on the synaptic markers. And one of the most exciting things at AAIC is Phospho-tau as a temporal treatment marker. Where does synaptic markers fit in there? Are they early? Are they late? You've done a lot of work to measure them. Are they useful treatment markers? And then, I have a INKmune follow-up.
Raymond Tesi: CJ, I'll let you handle this one. It's a fairly sophisticated question. Go ahead.
Christopher Barnum: Thanks, RJ. Hi, Tom. So I'm not sure they're a long-term solution as it relates to biomarker measurement. It's something you can do if you collect CSF, which is where the analysis was performed. It hasn't really translated to blood yet. But what we know about synaptic proteins and synaptic dysfunction and synaptic loss in Alzheimer's, we've actually known for quite a while that there's been a little bit of a resurgence to this at this point. And I think that's something that we can take advantage of. The other thing is it aligns really nicely with EEG. So changes in EEG are likely to be subserved by changes at the level of the synapse as opposed to an improvement in cell building or even axons as well, because it tends to be a little bit faster. But EEG is a nice surrogate outcome for that. I would say that while they're great they add to the story, they're probably not a long-term biomarker solution, but it does reinforce the biology of what we understand XPro can do. And I think that's really exciting to us because it targeted really what we were able to show is that we saw broad changes and networks of proteins that are critical for synaptic function. So to us, it's another biomarker to help support our decision-making and that we're -- the biology is aligning as we expect. But I don't know, aside from maybe EEG in the future that the biomarker proteins themselves are particularly useful in later stages.
Tom Shrader: Got it. And then, Mark, where are you -- or is it a priority to try to understand what is in INKmune that's driving the biology? It sounds like from the side effect profile, it's not a cytokine, which suggests it might be additive with cytokines. But do you have a sense of what it is? Is it a lot of things? Is it something that you might purify? Where are you on understanding what exactly INKmune depends on? Thanks.
Mark Lowdell: Yeah. That's a very good question, and I wish I knew all of the answers. But we've been looking at INKmune since 2005. So we've done a lot of work. And we initially thought exactly as you've alluded to, that we could find the magic signals that INKmune gives to the NK cell and make them artificially. What we did publish back in 2011 was that there -- INKmune is a cell. And obviously, it has millions of molecules on its surface. And they have -- those molecules, we found three that were absolutely critical to its function and they're published. What we tried to do was to produce an artificial version of those, and we were able to do that, but we could never get the concentrations. So imagine you've got three variables and each of those can be at different intensities, and we could never get the intensities right to be as good as the natural cell. The other thing that INKmune has that you could not reproduce artificially is that when INKmune binds to the NK cell, like any tumor cell, the NK cell rips a membrane out of INKmune. So INKmune is just a replication incompetent tumor cell. And it's the ripping out of that membrane, it's called trogocytosis, and its incorporation into the NK cell, which allows the NK cell that's being primed by INKmune, not only to function, but to go on and prime other resting NK cells. And we believe that's why we see such a long tail of effect after just three injections. So we haven't been able to find a way of producing an artificial version of INKmune. It's certainly a complex raft of proteins that come from the surface of the INKmune cell and they are incorporated into the NK cell in a way that making them artificially just wouldn't be able to provide that function. Having said that, INKmune is very cheap to manufacture and easy to ship. So...
Raymond Tesi: Yeah. And just I want to reemphasize your point about cytokines, Tom, because we think one of the really big deals about in INKmune is it doesn't require cytokines because as you said, the safety profile is markedly improved, and as Mark just implied, the cost profile was markedly improved. So we really like it, even though, as Mark said, he's still studying it, so.
Tom Shrader: Got it. Okay. Thank you.
Operator: [Operator Instructions] We'll take our next question from George Farmer with Scotiabank (TSX:BNS).
George Farmer: Hi. Good afternoon. Thanks for taking my questions. You mentioned the way you're enriching for enrollment in the Phase II AD trial, two things. One is selecting patients with specific biomarkers that would indicate a higher inflammatory state. And then also patients who will likely complete the study. The first one is understandable, but how are you enriching for the second?
Raymond Tesi: CJ?
Christopher Barnum: Yeah. So this is a great question. And there's really a couple of answers to that. And what I gave you was a simplified -- what you got was a simplified explanation. So the study itself, because we opted to go for a shorter study, six months, requires quite a bit of monitoring, probably much more so on a per day or per week basis, if you will, than you would see in other studies. There are sometimes where patients in other studies, they need to come in once a month. And in our study, you need to come in at least once a week, and we're doing multiple measurements as well. And so there -- that's going to be quite challenging for some patients to come in and do that. And so if we -- a lot of times what will happen is you enroll a patient and you end up with patients that miss visits or they end up leaving the study early. And of course, that creates problems as it relates to data analysis. So what we try to do at the very beginning is really have the conversation with the patients, let them -- get them to understand that the commitment is pretty high, and we really need their participation to make sure that they can complete all of those different things. And I think to the testament of our investigators, they've done a really good job to make sure that the patients that get into the trial are really willing to make that commitment. And we're seeing that in our retention rate as well. But we have had a number of patients at the beginning that say, what, I'm not sure that I can do that. And from our perspective, it's easier for us to move on. The other thing -- the other aspect of that is we're a little more rigid as it relates to the clinical diagnosis criteria of MCI and mild AD than we would normally be, again, because we have a small study. And believe it or not, there's quite a bit of variance in -- across investigators in what mild AD is and what MCI is in terms of diagnosis. And in order to compare apples-to-apples, we have to try to homogenize that. That's not a problem when you get to a Phase III study where you have more patients, you can relax some of that criteria. But those two things really do force us to slow enrollment and be more selective for patients, and it takes a little bit longer. The biomarker enrichment as it relates to inflammation is about what we expected it to be. I don't have the exact numbers on hand right now, but it is somewhere around 40% to 55% of those patients that show up have those biomarkers.
George Farmer: And then regarding those biomarkers, how do those patients fare relative to the general populations with respect to, say, baseline characteristics?
Christopher Barnum: In terms of their -- for example, their cognitive...
George Farmer: Yeah. Cognitive...
Christopher Barnum: So, good question. Obviously, I don't have that exact data for the study here. But generally speaking, what I can tell you is patients that have biomarkers of inflammation, if you look at the registry databases, they have more severe disease. They have faster progressing disease. And what's really unusual and really works in our favor is that the variance in progression between patients that have these biomarkers is smaller. So this allows us, again, to do these shorter trials with fewer patients.
George Farmer: Okay. Thanks very much.
Operator: And we have received a question from the web. And it reads, CJ, you seem excited about the interim data. How does this update, even though it's blinded, give your insight into how the trial is progressing?
Christopher Barnum: Yeah. So this is a great question. And I get this -- I've gotten this question quite a bit, is why is blinded data so exciting. I think the biggest challenge when you're in a new area is, especially when you're using biomarkers and you're selecting patients that really hasn't been done before, is when you go to power this study is the sample size that you use really representative of the patients out there. I mean, you only have the data that's available to go on to do that. And of course, that's a sample. And so the biggest question is -- to me is, a, do we have the right test? Can we capture those things? And is it performing as we expect? In other words, are we going to be able to -- is it accurately powered? And to not only see that was the case that the variances that we expected was there, but even numerically better and the quality of the data that we're able to collect, and in some ways, I'm maybe more excited about that because we review -- we record every single assessment and we review it. And if there are errors, we fix them quickly. So the teams that are in charge of reviewing and reaching out to sites and training and working with investigators, they help us with, it really is incredible. And what I can tell you is the independent consultants that we had, a neuropsychologist, that reviewed this said this is the highest quality data that they've seen, and that's all you can ask for. It means we have done absolutely everything we can do within our control and that's what really excites me about that.
Operator: And there are no further questions on the line at this time. I will turn the call to Dr. Tesi for any additional or closing comments.
Raymond Tesi: Thank you. As all of you know, the success in biotech depends on sound science, committed investors and medical need. The Alzheimer's space is added by the intrigue of honest disagreements on the value of recently approved drugs. We see real opportunity for XPro in Alzheimer's disease as these other drugs are better understood. And INKmune brings a unique perspective to the castrate-resistant prostate cancer arena because of its safety profile. There are drugs in development for metastatic castrate resistant prostate cancer. But you're not talking about young patients and these drug cocktails tend to be quite toxic. So safety matters in patients like that. Both of our platforms also show promise beyond their current indications. We've talked about treatment-resistant depression in Alzheimer's with XPro and other solid tumors with INKmune. Look no further than our website to see more than 80 publications that point to the many uses of these drugs. But at the end of the day, our aim is to provide data readouts on both of these programs as quickly as we can. We are grateful for shareholder support. We believe the future is bright. Thank you.
Operator: This does conclude today's program. Thank you for your participation, and you may now disconnect.
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