INmune Bio Inc (INMB) 2021 Q4 法說會逐字稿

Greetings, and welcome to the INmune Bio Fourth Quarter and Full Year 2021 Earnings Call. (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 is my pleasure to introduce Mr. David Moss, Co-Founder and CFO of INmune Bio. Thank you, David. The floor is yours.

Thank you, John, and good afternoon, everybody. We thank you for joining us for the call for INmune Bio's fourth quarter and full year 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 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 earnings press release, as well as the 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 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 Tesi, Co-Founder and CEO of INmune Bio. RJ?

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 [fourth] quarter and subsequent period, we will then move to Q&A. Starting with XPro. During 2021, we provided extensive detail of our clinical programs in Alzheimer's disease, including the results of the Phase I trial and the design of our Phase II programs in Mild AD and MCI or Mild Cognitive Impairment, a prodromal form of a Alzheimer's disease. The Phase I trial exceeded expectations. The study showed that XPro 1 milligram per kilogram once a week as a subcu 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 AD -- with Alzheimer's disease who have biomarkers of inflammation and neuroinflammation.

The Phase I trial demonstrated downstream benefits of decreasing neuroinflammation, including decrease in neurodegeneration or nerve cell death, improve synaptic function, arguably the most important target in Alzheimer's disease and remyelination. We provided anecdotes of improved cognition in the Phase I trial, but definitive evidence of the effects of XPro on cognition in patients with ADi awaits the results of the blinded, randomized Phase II trials. The company understands and must deliver clinically relevant data in these trials. We have presented detailed descriptions of the ADi Phase II trials previously.

Here, I will highlight the 2 unique aspects of those trials, both use enrichment strategies to enroll patients and both use EMACC, that's capitalized EMACC to test cognition. EMACC stands for early Alzheimer's disease cognition composite. EMACC is ideally suited to measure cognitive changes in patients with MCI and Mild AD. EMACC is a highly sensitive index of cognitive change composed of validated neuropsychological test measures. EMACC is psychometrically better suited to the early and mild range of illness than measures such as ADAS-Cogs. ADAS-Cogs suffers from a floor effects, which means that 9 of the 13 elements are at a ceiling effect, which means that 80% of the MCA patient -- MCI patients basically perform them flawlessly. This renders ADAS-Cogs insensitive to measuring changes in performance in these early AD populations.

Finally, EMACC 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, EMACC 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 that -- of cognition. Enrichment strategy is a term coined by the FDA and is commonly used in ALS and oncology trials. Enrichments means that 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 neuroinflammation. 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 risks. Because dementia in patients with ADi progresses both rapidly and reliably, I'll repeat, rapidly and reliably, the 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 I trial that showed that the response to XPro happens quickly in patients with mild disease, we designed the MCI and Mild AD trials to last 3 or 6 months respectively. Please refer to previous press releases, webinars on the website for more details. The mild Alzheimer's Phase II 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 will be 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 8 presentations at the 2 of the most important medical meetings for Alzheimer's disease, the AAIC and CTAD. We expect 2022 to be equally productive. In 3 weeks' time, INmune Bio is part of at least 4 presentations at the upcoming AD/PD meeting, the largest Alzheimer's meeting in Europe. We expect to maintain a high profile at the AAIC and CTAD in 2022. One of the bigger advantages of XPro to target neuroinflammation is that XPro can be used to treat a wide variety of neurodegenerative and neuroinflammatory diseases.

We have announced the Phase II trial in treatment-resistant depression, funded by the NIH, partially funded by the NIH. This third Phase II study with XPro will be initiated in 2022. Other diseases remain on the horizon, but more of that in the future. Before getting on to INKmune, I want to highlight the exciting research using INB03. INB03 is the DN-TNF program focused on oncology, and I'll remind you that was our first Phase I clinical trial several years ago. MUC4 or MUC4 is a proteoglycan expressed on the surface of many solid tumors. Roxana Schillaci has discovered that MUC4 is a biomarker for resistance to immunotherapy. Data with INB03 presented -- data using INB03 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 2 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. INB03 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 2 parallel tracts, and I have to say this is one of the more exciting innovations in the last 6 months. The first tract is that trastuzumab-based drug conjugates or [Tras ADCs], the most prominent being -- and HER2 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 [Tras ADC] tumors. [I might go a little fast], in breast cancer tumors -- in animal models, MUC4 expression prevents binding of trastuzumab to HER2/neu making them resistant to therapy.

MUC4 expression is driven by soluble TNF. So when you give INB03, MUC4 expression decreases and the tumor becomes sensitive to therapy. Resistant 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 AACR 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 INKmune program.

One clear difference of our INKmune 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 NK -- with cancer. INKmune 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 tools -- 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. INKmune changes the patient's innate resting NK cells into memory-like NK cells.

Memory-like NK cells are the cells that matter because they are 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, IL-15 and IL-18. Because this combination is too toxic to give to patients, this conversion must be done ex vivo in a test tube process that is costly and logistically complex. In 2021, we translated INKmune from bench to man, 3 patients with hematologic malignancies have been treated with INKmune, what have we learned? First, INKmune is safe and well tolerated. Each of the 3 patients received a single course of INKmune that is 3 simple intravenous infusions over a 2-week period.

INKmune has given as an outpatient and does not require pre-medication conditioning therapy or extra cytokine therapy. INKmune is simple and can be used in any center that treats cancer patients. INKmune performed 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, if 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 INKmune, they do.

Finally, both increase in -- 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 persistent lasted at least 12 weeks, that's at least 10 weeks longer beyond the last infusion of INKmune. This is promising. The science is great, but how are the patients doing? Of the 3 patients treated, 2 significantly improved with INKmune. The patient from the high-risk MDS trial shows decreased blast, decreased transfusion requirements and improved performance status. Before treatment, he was in bed for half the day as an ECOG2, now he is ECOG0, living a normal life, and for him, a normal life means [playing badminton].

The young woman with a failed bone marrow transplant with relapsed AML remains home with stable disease after a course of INKmune. 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 2 bone marrow transplants due to AML remains in the hospital. This week, the high-risk MDS program has been peer reviewed by the U.K. National Cancer Research Institute, Myelodysplastic Syndrome Expert Group. This group has accepted the trial for listing on the U.K. National MDS trial site. The NCRI scheme is unique to the U.K., no equivalent system exists in the U.S. The NCRI classification allows centers to refer patients to the -- to existing U.K. trial sites for treatment under the existing program.

Without this national listing, the patients must be treated in their local health care facilities. There's no ability to refer patients elsewhere. This we hope will improve enrollment. We also hope that this added validation and the exposure to the expert centers that the process entail will provide more patients for the clinical trial now and in the future. Professor Lowdell'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 promised the company recognizes the problem. The main delay in the Alzheimer's disease Phase II trials has been due to XPro drug supply. Because of COVID-related supply chain issues, new XPro was not available until January 2022. This was a 4-month delay. Every element of the Alzheimer's disease Phase II program was affected by this 4-month delay.

Now we have 25,000 doses of XPro 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-resistant depression and beyond. The XPro 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 an 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 2 additional employees to supplement our existing team to speed site initiations.

Finally, we have made an important change in the MCS -- MCI trial. Bear with me for this on a moment. Last year, we committed to positioning XPro for accelerated approval in Alzheimer's disease if Lilly followed a Phase II accelerated approval regulatory path with donanemab, they are promising anti-amyloid therapy. The CMS decision on January 11 made it clear that Phase II programs will most likely be required. This decision impacted our development plans.

We have altered the design of the Phase II trial in MCI. It will now be a 2-arm trial previously, it was a 3-arm trial, comparing 12 weeks of 1 milligram of XPro to placebo, 60 patients enrolled in a 2:1 ratio. There will be no patients enrolled at 2 milligram per kilogram. The elimination of the 2 milligram per kilogram arm allows us to eliminate invasive diagnostic and biomarker assays that will -- 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 II trial have changed. The time from first patient to 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. INKmune 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, it allows other expert centers in the U.K. 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 U.K. Our goal is simple, get 8 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.

Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones before we head to our Q&A session. Net loss attributable to common stockholders for the year ended December 31, 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 31, 2021 compared to $0 million 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 31, 2021 was approximately $1.2 million compared to $0.1 million of other income during the year ended December 31, 2020. The increase in other expenses was mainly due to the company incurring interest expense on the debt, which is used to purchase back equity.

At December 31, 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 3, 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 XPro Phase II program for Mild Cognitive Impairment in patients with APOE4 allele in the first half of 2022. We plan to initiate XPro 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 INKmune Phase I program in ovarian cancer in the second half of 2022. And we plan additional open-label Phase I trial data of INKmune in high-risk MDS patients. We plan to report top line data from the Phase II trial of XPro in MCI patients in the first half of 2023. And we plan to report top line data from the Phase II trial of XPro in mild Alzheimer's patients in the second half of 2023. We also plan to present INKmune clinical data and new preclinical data on mechanism of action at the Innate Killer Summit conference in San Diego in March.

We also plan to report preclinical INKmune data in at least 2 new solid tumor indications, renal cell carcinoma and nasopharyngeal carcinoma. We also plan Oral and Poster presentations at AD/PD 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 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.

(Operator Instructions) Our first question comes from the line of Tom Shrader with BTIG.

Thanks for the update on the XPro supply, solved some questions. I have 2 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.

So, well, I'm going to answer the 2 questions 2 ways. First of all, we agree with your assessment that a lot of the data are cellular. But there's -- if you look at the original work out of Washington University and Holtzman company, who actually described APOE4, these patients do appear to be inflamed. And when you look at our data, which our particular interest in drilling down on the incidence of neuroinflammation, actually, the patients that are APOE4 positive in our Phase I 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.

Yes, interesting. Okay. And then I'm wondering if you could give us -- can you tease apart EMACC 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?

Yes. No, I'm not -- yes, that's a good question. I'm not the person to give the deep dive. But I will say that Judy Jaeger 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 is actually was one of the driving forces on this. When she gathered basically working with companies, it was clear that they were -- that the traditional endpoints weren't good for Mild, let's call early AD patients.

So, and early AD by the way is MCI and Mild patients. They spent a huge effort looking at, I think, 4 different databases and analyzing this to come up with a set of criteria, it is a set of criteria, 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 ADAS-Cog, better than CDR. Now there are publications on this, and the best thing to do is to talk to Judy, who is very articulate on this. I'm 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 ADAS-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.

Okay. Thanks for the input.

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

Thank for the detailed update and appreciate you taking the question. So 2 parts for AD. Maybe if you could orient ourselves to 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 have a follow-up on [next].

On your first question, we've been primarily mining the Phase I trial. As you know, if you've ever heard us talk, we got a boatload of data and much of its [premium] data and we will continue to mine that. Do I think there's a lot new there, no. If you listen to what we've 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 or less nerve cell death, improve 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 AD/PD, quite frankly, is to begin to expose ourselves to the clinical teams in Europe. AD/PD 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, Mayank.

Yes, maybe I can follow up offline. Just as you know, GLP-1 receptor agonist has anti-inflammatory effects, and there was a recent 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, 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, central peripheral inflammation are lifestyle issues associated with diabetes and obesity, right, and metabolic syndrome, all of those are really in the same bucket. So the GLP-1 study clearly affects peripheral inflammation. And we -- 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 suggested that, it should. And I will add that one of the advantages of XPro versus more targeted therapies that only target neuroinflammation is that not only can we target neuroinflammation with XPro. But we also target what is driving neuroinflammation, which are the peripheral causes associated with intestinal leak, obesity, et cetera. So yes, we think that kind of stuff is very supportive of what we're doing. We love it.

Yes. No, I figured. And on the Phase II 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?

Yes, and it really didn't change. The way we designed it, it wasn't -- remember, the role of the 2 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 I and all of the biomarker data that we have, that 1 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 -- and increases -- it improves it a little bit of 1 milligram over placebo. The main advantage is it eliminates the barrier of the invasive studies, now 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. And just one quick question on the MDS oncology side. There are, to my understanding, 2 patients treated under compassionate use. So is there any biomarker or anti-tumor response data that you may have from that, as you provided for, I think one patient before?

Well, we don't have the extensive biomarker data we had in the MDS patients, because as a compassionate use, you -- the U.K. is quite strict about what labs you can draw. We have clinical data, a patient was in hospital requiring antibiotics who -- 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 2 transplants, I can't say whether we gave him -- whether he benefited from XPro or not, but the young lady definitely benefited. And we were predicting she was going to need to be re-transplanted before Christmas, and we're 4 months late, right? So who knows what's going to happen, right?

Our next question comes from the line of Matthew Cross with Alliance Global Partners.

I appreciate the thorough status update, and thanks for taking a couple of questions from me. So I had one each on XPro and INKmune. So, first of all, on XPro, just wanted to clarify kind of stemming off of Tom's question earlier about the MCI trial. I know -- I think we recently saw that Roche has announced this trial that, 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 -- there were some inclusion criteria around the CDR and ECOG scores, some kind of baseline cognitive metrics. So just wanted to confirm whether it was all around APOE4 and biomarkers now as you're looking ahead? And then I have a kind of 2-part follow-up on INKmune.

Yes. 2, 3 elements, important elements there. The definition of whether you have MCI, mild, moderate or severe is based on cognitive testing. So that space -- so basically, you get categorized of how severe you are based on whether you're -- whether it be EMACC or ADAS-Cog or CDR or MMSE, for instance, MMSE is the crudest of these measures. But that's -- that really puts you in the bucket, right, which bucket are you in, in MCI or Mild. And so the next thing we do [is in our view of] neuroinflammation. And that's where we have -- we draw tests of the blood, which actually show that in the MCI trial if you're APOE4 positive or not or in the Mild trial, you have mild or whether you have metabolic syndrome, et cetera.

So those 2 elements, it's like a 2-step process. The -- there will be MCI patients and Mild patients that are not eligible for our trial. Now the Roche trial is different. The Roche trial is patients who are amyloid positive, but are normal -- I -- by the way I understand it, are do not have MCI, in other words, aren't 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 [proof of prevention] trial. And as you know from their press release, it's a 5-year trial, which means it's probably a 7-year trial before they have a result. 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.

Understood. No, that's super helpful clarification and distinction, RJ. Appreciate it. And then like I said, there's kind of a 2-part question around INKmune. 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 INKmune. It sounded like there -- some of your patients in a number of cases had been transplant experience. So I was curious if that transplant angle means anything to you or would you kind of anticipate that the benefits of INKmune are equally relevant whenever that's introduced in the course of treatment for leukemia?

So we have expressively gone in the hematologic malignancy space, we have expressively gone after MDS 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 -- 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 INKmune is in solid tumors. And I'll 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 I 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 -- as Wayne Gretzky said, what made him great is he used the puck to -- he used the skate 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.

Fair enough. Okay. No, yes, looking forward to all the preclinical data from that program and the ovarian program. So thanks for the commentary. Really appreciate it.

At this time, we've reached the end of the question-and-answer session. And I'll now turn the call back over to RJ for any closing remarks.

So we thank you for listening. I want to reemphasize that we as a company are quite -- on one hand, we're excited about the progress on -- we've made, on the other hand, we are tremendously frustrated as you are by some of these hiccups and enrollments. And we're the first to admit they are a problem. I think today, it was the first time we made it clear that part of the XPro problem was related to manufacturing delays, which are always a daunting problem for any biologic. But the bottom line is we are working hard. We'll 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. So with that, we thank you.

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.