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spk05: Greetings and welcome to the ImmuneBio fourth quarter and full year 2021 earnings call. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it is my pleasure to introduce Mr. David Moss, co-founder and CFO of ImmuneBio. Thank you, David. The floor is yours.
spk06: Thank you, John, and good afternoon, everybody. We thank you for joining us for the call for ImmuneBio's fourth quarter and full year 2021 financial results. With me on the call is Dr. RJ Tessie, CEO and co-founder of ImmuneBio, who will provide a business update on our clinical programs. 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 earning press release, as well as the 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 of the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, Immune Bio disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. With that out of the way, now I'd like to turn the call over to Dr. RJ Tessie, co-founder and CEO of Immune Bio. RJ.
spk04: Thank you, David, and thank you, everyone, for joining the call. As is our practice, I will arrange my remarks to highlight key takeaways for the first quarter. and subsequent period. We will then move to Q&A, starting with EXPRO. During 2021, we provided extensive detail of our clinical programs in Alzheimer's disease, including the results of the Phase 1 trial and the design of our Phase 2 programs in mild AD and MCI, or mild cognitive impairment, a prodromal form of Alzheimer's disease. The Phase 1 trial exceeded expectations. Studies showed that Expro, one milligram per kilogram once a week as a sub-Q injection, decreases neuroinflammation in patients with ADI. That's capital A, capital D, small i. ADI is the term we have coined for patients with Alzheimer's disease who have biomarkers of inflammation and neuroinflammation. The phase one trial demonstrated downstream benefits of decreasing neuroinflammation, including decreased neuroinflammation. or nerve cell death, improved synaptic function, arguably the most important target in Alzheimer's disease, and remyelination. We provided anecdotes of improved cognition in the phase one trial, but definitive evidence of the effects of XPRO on cognition in patients with ADI awaits the results of the blinded randomized phase two trials. The company understands it must deliver clinically relevant data in these trials. We have presented detailed descriptions of the ADI phase two trials previously. Here I will highlight the two unique aspects of those trials. Both use enrichment strategies to enroll patients and both use EMAC, that's capitalized E-M-A-C-C, to test cognition. EMAC stands for Early Alzheimer's Disease Cognition Composite. EMAC is ideally suited to measure cognitive changes in patients with MCI. and mild AD. EMAC is a highly sensitive index of cognitive change composed of validated neuropsychological test measures. EMAC is psychometrically better suited to the early and mild range of illness than measures such as ADES-COGS. ADES-COGS suffers from a floor effect, which means that nine of the 13 elements are at a ceiling effect, which means that 80% of the MCI patients basically perform them flawlessly. This renders ADES-COGS insensitive to measuring changes in performance in these early AD populations. Finally, EMAC is being used by other companies in AD trials, and we believe it will become the standard endpoint for cognition in clinical trials in this group of patients. Put simply, EMAC is the best tool for the task. I believe that many of the failures of AD drug development in the past have been partly caused by the use of the historically crude measures of cognition. Enrichment strategy is a term coined by the FDA and is commonly used in oncology trials. Enrichment means the use of biomarkers to select patients for a clinical trial to match their disease with the drug therapy. Basically, you're slanting the trial to success. Our CNS trials are enriched for patients who have neuroinflammations. This distinct ADI subset equals about half of the Alzheimer's disease patient population. The ADI enrichment strategy provides trial design advantages that improve efficiency and decrease risk. Because dementia in patients with ADI progresses both rapidly and reliably, I'll repeat, rapidly and reliably, that clinical trials are shorter and smaller than trials that do not use enrichment strategies. Combining findings from publicly available databases, such as the ADNI database of the USC, with data from our phase one trial that showed that the response to EXPRO happens quickly in patients with mild disease, we designed the MCI and mild AD trials to last three or six months, respectively. Please refer to previous press releases, webinars, and the website for more details. The MILD Alzheimer's Phase 2 trial is actively screening patients. We will announce when we have treated our first patient. The MCI trial will start in a few months, and we remain confident that the top-line data we reported in the first half of 23 for the MCI trial the second half of 23 for the MILD-AD trial. In 2021, we contributed eight presentations at the two of the most important medical meetings for Alzheimer's disease, the AAIC and CTAD. We expect 2022 to be equally productive. In three weeks' time, Immune Bio is part of at least four presentations at the upcoming ADPD meeting, the largest Alzheimer's meeting in Europe. We expect to maintain our high profile at the AAIC and CTAD in 2022. One of the bigger advantages of EXPRO to target neuroinflammation is that EXPRO can be used to treat a wide variety of neurodegenerative and neuroinflammatory diseases. We have announced a phase two trial on treatment-resistant depression funded by the NIH, partially funded by the NIH. This third phase two study with EXPRO will be initiated in 2022. Other diseases remain on the horizon, but more of that in the future. Before getting on to IncMUNE, I want to highlight the exciting research using MbO3. MbO3 is a DN-TNF program focused on oncology, and I'll remind you that was our first Phase I clinical trial several years ago. Mucin-4, or MUC4, is a proteoglycan expressed on the surface of many solid tumors. Roxana Solaci has discovered that MUC4 is a biomarker for resistance to immunotherapy. Data using MbO3 in breast tumors expressing MUC4 have been presented at the San Antonio Breast Cancer Symposium in 2020-2021, and the publication list is long and growing. Those posters and publications are available on our website. Why is this program important? We believe two of the biggest trends in cancer immunotherapy is resistance to immune checkpoint inhibitors and innovations in trastuzumab-based therapies. Resistance to checkpoint inhibitors is about the immunobiology of the tumor microenvironment. MbO3 appears to make cold tumors hot and may convert a tumor resistant to checkpoint inhibitors to one that is sensitive to checkpoint inhibitors. The expanding role of trastuzumab-based therapies is following two parallel tracks, and I have to say this is one of the more exciting innovations in the last six months. The first track is that trastuzumab-based drug conjugates, or TRAS-ADCs, the most prominent being NHER2, are being used a lot. The second is the expanding use of TRAS-ADCs in low-expressing HER2-neu tumors. The breast cancer expansion in low-expressing tumors more than doubles the number of patients who may benefit from TRAV-ADC tumors. In breast cancer tumors, in animal models, MUC4 expression prevents binding of TRAV-Tuzumab to HER2-neu, making them resistant to therapy. MUC4 expression is driven by soluble TNF, so when you give NbO3, MUC4 expression decreases, and the tumor becomes sensitive to therapy. Resistance to TRAS-ADC is now being reported in patients, and we expect this conversation to continue and expand over the next year or so. Additional data will be presented at this year's AHCR, and our presence at San Antonio Breast Cancer Symposium will continue. The third, in our opinion, the third big trend in oncology is the increased importance of NK cells. And this is a great segue into our InCommune program. One clear difference of our InCommune program compared to other NK programs is that we do not give NK cells. I repeat, we do not give NK cells, but aim to improve the function of the abundant NK cells in patients with cancer. InCommune is a universal, off-the-shelf therapy with cost-effective manufacturing that activates the patient's own NK cells. I say that again. We believe the patient's NK cells have all the tools they need to kill the cancer, but they lack the signals necessarily to initiate that process. Most patients have plenty of NK cells that just don't work. Inquimune changes the patient's inert resting NK cells into memory-like NK cells. Memory-like NK cells are the cells that matter because they're the NK cells that kill cancer. It's possible to make memory-like NK cells from cytokines, but this requires a triple cytokine cocktail of IL-12, 15, and 18. Because this combination is too toxic to give to patients, This conversion must be done ex vivo in a test tube, a process that is costly and logistically complex. In 2021, we transplanted IncMune from bench to man. Three patients with hematologic malignancies have been treated with IncMune. What have we learned? First, IncMune is safe and well-tolerated. Each of the patients received a single course of IncMune, that is three simple intravenous infusions over a two-week period. Incomune is given as an outpatient and does not require premedication, conditioning therapy, or extra cytokine therapy. Incomune is simple and can be used in any center that treats cancer patients. Incomune performs better than expected in patients. A high percentage of the patient's resting NK cells are converted to the cancer-killing memory-like phenotype, the only NK cells that matter in patients with cancer. The patient's memory-like NK cells kill NK-resistant cancer cells in a laboratory assay. That's to say it's one thing to change the phenotype. It's another thing to make sure that those cells now kill cancer. Before treatment, the patient's NK cells did not kill cancer. After income, they do. Finally, both the increase in memory-like NK cells and the cancer killing lasted for many weeks. We call this therapeutic persistence. In the MDS patient, therapeutic persistence lasted at least 12 weeks. That's at least 10 weeks longer beyond the last infusion of vincmium. This is promising. The science is great, but how are the patients doing? Of the three patients treated, two significantly improved with vincmium. The patient from the high-risk MDS trial shows decreased blasts. decreased transfusion requirements, and improved performance status. Before treatment, he was in bed for half the day as an ECOG-2. Now he's ECOG-0, living a normal life, and for him, a normal life means playing badly. The young woman with a failed bone marrow transplant with relapsed AML remains home with stable disease after a course of incoming. She may still need a second transplant, but the urgency surrounding that decision has been mitigated. The third patient, a young man who has failed two bone marrow transplants due to AML, remains in the hospital. This week, the high-risk MDS program has been peer-reviewed by the UK National Cancer Research Institute Myelodysplastic Syndrome Expert Group. This group has accepted the trial for listing on the UK National MDS trial site. The NCRI scheme is unique to the UK. No equivalent system exists in the US. The NCRI classification allows centers to refer patients to existing UK trial sites for treatment under the existing program. Without this national listing, the patients must be treated in their local healthcare facilities. There's no ability to refer patients elsewhere. This, we hope, will improve enrollment. We also hope that this added validation and exposure to the expert centers that the process entails will provide more patients for the clinical trial now and in the future. Professor Liddell's team continues to dig deeper into how does this work and why is this better than cytokine questions. In 2022, his team will release data at meetings on these questions. Now to the elephant in the room. Why have clinical trial enrollment been slowed and delayed? I promise the company recognizes the problem. The main delay in the Alzheimer's disease phase two trials has been due to expo drug supply. Because of COVID related supply chain issues, new expo was not available until January 2022. This was a four-month delay. Every element of the Alzheimer's disease phase two program was affected by this four-month delay. Now we have 25,000 doses of Expro on hand with another 40,000 doses of drug in the process, in process, so to speak, that will support for future and further development in Alzheimer's treatment resistance, depression, and beyond. The expo drug supply problem is behind us, but the consequences of that delay is the delayed start dates. To make up lost time, we have engaged in international CRO with deep experience in managing Alzheimer's disease trials. We plan to open 45 sites in the mild AD trial and 25 sites for MCI. 85% of the sites will be enrolling both trials. We have hired two additional employees to supplement our existing team to speed site initiations. Finally, we have made an important change in the MCI trial. Bear with me for this on a moment. Last year, we committed to positioning ExPro for accelerated approval in Alzheimer's disease if Lilly followed a phase two accelerated approval regulatory path with Donamimab, their promising anti-amyloid therapy. The CMS decision on January 11th made it clear that phase two programs will most likely be required. This decision impacted our development plans. We have altered the design of the phase two trial in MCI. It will now be a two-arm trial. Previously, it was a three-arm trial. Comparing 12 weeks of one milligram of Expro to placebo. 60 patients enrolled in a two-to-one ratio. There will be no patients enrolled at two milligram per kilogram. The elimination of the two milligram per kilogram arm allows us to eliminate invasive diagnostic and biomarker assays that were going to be a barrier, so to speak, to enrollment. The trial endpoints, the statistical power, none of the other elements have changed, and none of the elements of the mild AD phase two trial have changed. The time from first patient enrolled to the last patient enrolled in the MCI trial should be improved with the elimination of these invasive tests. In summary, we expect, as we have in the past, that the Phase II trials in MCI and mild AD will report top-line data in the first half of 23 and the second half of 23, respectively. That is, The MCI trial will report in the first half of 23, and the mild AD trial will report in the second half of 23. IncMUNE is equally frustrating. I mentioned one benefit of the NCRI classification is that centers can refer patients to clinical sites outside of their catchment area. The second benefit is it allows other expert centers in the UK to join the program as a clinical site. We hope the NCRI classification enlarges the pool of eligible patients for this high-risk MDS trial. We are also looking to expand into sites outside of the UK. Our goal is simple. Get eight additional patients enrolled by the end of 2022. With that, I will turn it over to David Moss, our CFO, to review certain financial items.
spk06: Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones before we head to our Q&A session. Net loss attributable to common stockholders for the year ended December 31st, 2021 was approximately $30.3 million compared with approximately $12.1 million for the full year of 2020. Revenues totaled $0.2 million for the year ended December 31st, 2021 compared to zero for the year ended December 31, 2020. Research and development expenses totaled approximately $20.5 million for the year ended December 31, 2021, compared with approximately $5.9 million for the full year of 2020. The primary reason for the increase in expenses was an increase in clinical trial costs as we prepare for these Phase II AD programs. and an increase in costs associated with manufacturing of additional DN, TNF drug supply, as RJ mentioned just earlier. General and administrative expense was approximately $8.8 million for the full year ended December 31, 2021, compared to $6.3 million for the full year of 2020. The increase in G&A is mainly due to higher compensation expense, including stock-based compensation and higher consulting fees. Other expenses for the year ended December 31st, 2021 was approximately 1.2 million compared to 0.1 million of other income during the year ended December 31st, 2020. The increase in other expenses was mainly due to the company incurring interest expense on the debt, which it used to purchase back equity. At December 31st, 2021, the company had approximately 74.8 million of cash. Based on our current operating plan, we believe our cash is sufficient to fund our operations into 23. As of March 3rd, 2022, the company had approximately 17.9 million shares of common stock outstanding. Now I'd like to move on and list our upcoming milestones and catalysts. Our upcoming milestones. We plan to initiate Expro Phase 2 program for mild cognitive impairment in patients with APOE4 allele in the first half of 2022. We plan to initiate EXPRO Phase II program for treatment of resistant depression, TRD, funded in part by a $2.9 million NIH grant by the second half of 2022. We plan to initiate IncMUNE Phase I program in ovarian cancer in the second half of 2022. And we plan additional open-label Phase I trial data of IncMUNE in high-risk MDS patients. We plan to report top line data from the phase two trial of EXPRO and MCI patients in the first half of 2023. And we plan to report top line data from the phase two trial of EXPRO in mild Alzheimer's patients in the second half of 2023. We also plan to present immune clinical data and new preclinical data on mechanisms of action at the innate killer summit conference in San Diego in March. We also plan to report preclinical immune data and at least two new solid tumor indications, renal cell carcinoma and nasopharyngeal carcinoma. We also plan oral and poster presentations at ADPD 2022, the largest European AD meeting. The meeting will be held in Barcelona in March. So in summary, we're pleased with our progress during the fourth quarter as we continue to advance our pipeline towards potentially evaluating and creating milestones. At this point, I'd like to thank you for your time and attention. I'd like to turn it back to John to poll for questions. John.
spk05: Thank you, David. At this time, we will be conducting a question and answer session. If you would like to ask a question, please press star 1 on your telephone keypad. A confirmation tool will indicate that your line is in the question queue. You may press star 2 if you would like to remove your question from the queue. And for participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we poll for questions. Our first question comes from the line of Tom Schrader with BTIG. You may proceed with your question.
spk02: Good afternoon. Thanks for the update on the X-Pro Supply. It solves some questions. I have two questions. The first one is on the use of ApoE as a marker. At least at a cellular level, APOE is being increasingly implicated as being inflammatory. Is there clinical data to support that yet? Are essentially all APOE patients going to be inflammatory? Do we know yet? I'm just curious what you guys know because the data we've seen is mostly cellular.
spk04: So, well, I'm going to answer the question two ways. First of all, we agree with your assessment that a lot of the data are cellular. But, you know, there's, if you look at the original work out of Washington University and Holtzman and company who actually described ApoE4, these patients do appear to be inflamed. And when you look at our data, which, you know, our particular interest in drilling down on the incidence of neuroinflammation, Actually, the patients that are APOE4 positive in our phase one trial were hot, right? They were hot if you measured them looking at inflammatory cytokines, if you looked at white matter-free water. So we believe, in fact, that APOE4 is a biomarker that predicts inflammation in the patients. Now, whether that inflammation is independent of peripheral inflammation, we can't tell at this point. But we are very comfortable that, in fact, this is one of the driving, this is the genetic marker that we can easily identify that is identifying a group of patients that have neuroinflammation. And we like it so much that the only enrichment criteria or enrollment criteria for the MCI trial is you have to be ApoE4 positive.
spk02: Interesting. Okay. Thank you. I'm wondering if you could give us, can you tease apart EMAC and give us an intuitive sense of what's different about it that makes it better in these patients, or is it sort of in the realm of correlations and sort of beyond intuition. I'm just kind of curious if you give us some simple sense of why it's better.
spk04: Yeah, that's a good question. I'm not the person to give the deep dive. But I will say that, you know, Judy Yeager is our consultant on this. She had a presentation at CTAD on this. She had a presentation at AAIC. And in fact, she is a She actually was one of the driving forces on this. When she gathered basically, you know, working with companies, it was clear that the traditional endpoints weren't good for mild, let's call early AD patients. So, and early AD, by the way, is MCI in mild patients. They spent a huge effort looking at, I think, four different databases. and analyzing this to come up with a set of criteria. It is a set of criteria. It's not a single test, but a set of criteria that allows them to have a more sensitive measure of cognition that is better, certainly than ADS-Cog, better than CDR. Now, there are publications on this, and, you know, the best thing to do is to talk to Judy, who is very articulate on this. I am not the one to answer this in detail, but the point is clear that it is a better cognitive measure or sensitive measure in these milder patients, early patients, I guess, is a better way to do it. And that 8S-COG is like using a, as I said today, it's like trying to use a chainsaw to make a salad bowl. It's just not the right tool for measuring it in MCI and mild patients. So I didn't answer your question, but the data are very solid. I'm just not the best messenger.
spk02: Okay. Okay. Thanks for the input.
spk05: Our next question comes from the line of Mayank Mamtani with B. Reilly Securities. You may proceed with your question.
spk01: Good afternoon. Thanks for the detailed update and appreciate you taking that question. So two-part for AD. Maybe if you could orient ourselves to, you know, what should we be paying attention at the AD PD conference? Looks like you have many abstracts there. And also, if you're able to comment on the recent GLP-1 receptor agonist double-blind pretty large randomized controlled trials, data set put together, showing impact on dementia, and then I will follow up on experts.
spk04: on your first question we've been primarily mining the uh the uh phase one trial as as you know if you've ever heard us talk you know we got a boatload of data and much of its proteome data and we've been continue to mine that do i think there's a lot new there no do you know if you've listened to what we've uh said for the most part we're just refining what we said and because In fact, the messages are very clear. We know we decrease neuroinflammation. We know the downstream benefits of decreasing neuroinflammation are less nerve cell death, improved synaptic function, and remyelination. And we know that although we had hints of improved cognition because we didn't have a placebo group, we are, we cannot really comment on improvements of cognition until we do the blinded randomized trial. The main goal for us for getting going to the ADPD, quite frankly, is to begin to expose ourselves to the clinical teams in Europe. ADPD is an EU meeting. AAIC and CTAD are primarily U.S. meetings, and as you can imagine, AD is a global disease. I missed exactly what you were asking on your second question, ma'am.
spk01: Yeah, maybe I can follow up offline. Just as you know, GLP-1 receptor agonist has anti-inflammatory effects, and there was a recent study large database, both real world and from the double blind placebo controlled trials that was presented. That was interesting. So maybe I'll take that offline. No, no, no.
spk04: Let me answer that. I want to answer that. I do. I do. No. And let me tell you why, because it plays well, it plays into our thesis, right? Our thesis is that peripheral inflammation drives central inflammation, right? Full stop, right? And one of the greatest sources of proliferation of peripheral inflammation are lifestyle issues associated with diabetes and obesity, right? Metabolic syndrome. All of those are really in the same bucket. So the GLP-1 studies clearly affect peripheral inflammation. And I think we would have hypothesized that getting rid of peripheral inflammation with GLP-1 inhibitors would affect neuroinflammation. And there's evidence out there that suggests it may. It should. And I will add that one of the advantages of EXPRO versus more targeted therapies that only target neuroinflammation is that not only can we target neuroinflammation with EXPRO, But we also target what is driving neuroinflammation, which are the peripheral causes associated with, you know, intestinal leak, obesity, et cetera. So, yeah, we think that kind of stuff is very supportive of what we're doing.
spk01: We love it. Yeah, no, I figured. Thank you. And on the phase two MCI study, are you able to comment on the screen rate or failure rate? sort of relative expectation what you had before versus what you may have now that you have taken out the invasive biomarker component?
spk04: Yeah, it really didn't change. The way we designed it, it wasn't, remember the role of the two milligram group was to accelerate our path to getting a fixed dose strategy, right? If we were not testing a higher dose, because we're convinced based on our dose response in the phase one and all of the biomarker data that we have that one milligram is the dose, we were trying to shortcut a step to commercialization. So it really didn't, it doesn't change the power of this trial for looking at the benefit of the, it improves it a little bit, of one milligram over placebo. The main advantage is it eliminates the barrier of the invasive studies, and I'm talking about the LP. As you know, lumbar punctures are not necessarily coveted by patients, and by eliminating lumbar punctures, you increase the number of patients interested in joining the trial. Okay.
spk01: And just one quick question on the MDS oncology side. There are, to my understanding, two patients treated under compassionate use. So is there any biomarker or antitumor response data that you may have from that as you provided for, I think, one patient before?
spk04: Well, we don't have the extensive biomarker data we had in the MDS patients. Because as a compassionate use, the UK is quite strict about what labs you can draw. We have clinical data. A patient was in hospital requiring antibiotics and transfusion who has been discharged home off antibiotics, not requiring transfusion. She still has blasts, but they're stable. The young man, he failed two transplants. I can't say whether we gave him, whether he benefited from expo or not, but the young lady definitely benefited. And, you know, we were predicting she was going to need to be retransplanted before Christmas, and we're four months later, right? So who knows what's going to happen, right?
spk03: Okay.
spk01: Thanks for digging our questions.
spk05: Our next question comes from the line of Matthew Cross with Alliance Global Partners. You may proceed with your question.
spk00: Hi, guys. I appreciate the thorough status update, and thanks for taking a couple of questions from me. So I had one each on XPRO and InCommune. So first of all, on XPRO, I just wanted to clarify, you know, kind of stemming off of Tom's question earlier about the MCI trial. I know, you know, I think we recently saw that that Roche has announced this trial that is not screening based on cognitive symptoms or scores in that line of criteria, but solely on amyloid and kind of a biomarker strategy, which it sounds like is the direction you're leaning with MCI. I think previously it was my understanding that there was some inclusion criteria around CDR and ECOG scores, some kind of baseline cognitive metrics So I just wanted to confirm whether it was all around APOE4 and biomarkers now as you're looking ahead. And then I'll have a kind of two-part follow-up on InCommune.
spk04: Yeah, two or three elements, important elements there. You know, the definition of whether you have MCI mild, moderate, or severe is based on cognitive testing. So basically, you get categorized of how severe you are based on whether it be EMAC or ADES-COG or CDRs or MMSE, for instance. MMSE is the crudest of these measures. But that really puts you in the bucket, right? Which bucket are you in, an MCI or mild? And so the next thing we do is, do you have neuroinflammation? And that's where we have, we draw tests of the blood, which actually show that, you know, in the MCI trial, you're either ApoE4 positive or not, or in the mild trial, you have mild, or, you know, whether you have, you know, metabolic syndrome, et cetera. So those two elements are, It's like a two-step process. There will be MCI patients and mild patients that are not eligible for our trial. Now, the ROSE trial is different. The ROSE trial is patients who are amyloid positive, but are normal, the way I understand it, do not have MCI. In other words, have normal cognition. And they're trying to determine if they treat patients who are amyloid positive, if they will, it's basically preventing them from becoming MCI patients. Because as you know, MCI patients then slip into mild AD, et cetera. So that's a true prevention trial. And as you know from their press release, it's a five-year trial, which means it's probably a seven-year trial before they have results. And all I can say is they have the balance sheet that can do that kind of thing, and we wish them the best of luck.
spk00: Understood. No, that's super helpful clarification and distinction, RJ. Appreciate it. And then, like I said, I have this kind of two-part question around IncMUNE. Similarly, looking across the landscape, we've kind of recently seen data from peers in the NK cell therapy space indicating the potential benefits of pairing NK cell therapy in some fashion with stem cell transplant. which I bring up given the focus on high-risk MDS and leukemia generally, it sounds like, that you guys are focused on. So I guess as you continue to advance in high-risk MDS, I was wondering if you could comment on kind of the average lapse you're seeing. I know this is super early days enrollment-wise, but the average lapse you're seeing between best prior response and initiation of Incommune. It sounded like some of your patients in a number of cases had been transplant experienced. So I was curious if that transplant angle means anything to you, Or would you kind of anticipate that the benefits of ink moon are equally relevant whenever that's introduced in the course of treatment for leukemia?
spk04: So we have expressively gone, in the hematologic malignancy space, we have expressively gone after NDS because the therapeutic choices are less effective and poor. Most cell therapy companies, NK cell therapy companies, are going after AML. And that's why they often include these patients with who have had, you know, have had a transplant, have failed the previous line of therapy, et cetera, because that is where that has all worked out. Now, although we started in the hematologic malignancy, we have made it clear that we think the biggest opportunity for ink immune is in solid tumors. And I remind you that 90% of tumors are solid tumors. So the market opportunity is much larger. And I also point out that the competition is much lower. David mentioned that we have preclinical activity going on in nasopharyngeal carcinoma and renal cell carcinoma. We have announced an ovarian cell carcinoma phase one trial. So I think long term, I would think that we are going to be talking a lot more about solid tumors. And then these discussions about intervals and blast relapse, which are really hematologic malignancy concepts, are not relevant to our discussion. We're going, you know, you know, as Wayne Gretzky said, you know, what made him great is he used to escape to where the puck was going to be. We're skating to where we think the puck is going, which is solid tumors. We're not going to fight the battles in AML at this point.
spk00: Fair enough. Okay. No, yeah, looking forward to all the preclinical data from that program and the ovarian program. So thanks for the commentary. Really appreciate it.
spk05: At this time, we have reached the end of the question and answer session. And I'll turn the call back over to RJ for any closing remarks.
spk04: So we thank you for listening. I want to re-emphasize that we as a company are quite, on one hand, we're excited about the progress we've made. On the other hand, we are tremendously frustrated, as you are, by some of these hiccups in enrollments. And we are the first to admit they are a problem. I think today was the first time we made it clear that part of the expo problem was was related to manufacturing delays, which are always a daunting problem for any biologic. But the bottom line is we are working hard, we will do better, and we are confident that the trial designs that we've chosen will present results that will hopefully translate into increased value for investors.
spk03: So with that, we thank you.
spk05: This does conclude today's conference call. You may disconnect your lines at this time. Thank you for your participation and have a great day.
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