This conference call transcript was computer generated and almost certianly contains errors. This transcript is provided for information purposes only.EarningsCall, LLC makes no representation about the accuracy of the aforementioned transcript, and you are cautioned not to place undue reliance on the information provided by the transcript.
spk01: greetings and welcome to the immune bio third quarter 2023 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 and then 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, CFO of ImmuneBio. David, the floor is yours.
spk02: Thank you, Claudia, and good afternoon, everybody. We thank you for joining us for ImmuneBio's third quarter 2023 financial results. With me on the call is Dr. RJ Tessie, CEO of ImmuneBio, and Dr. Mark Liddell, Chief Scientific Officer of ImmuneBio, We'll provide an update on IncBUNE, our memory-like natural killer cell oncology platform. Before we begin, I remind everyone that except for statements of historical fact, 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 risk factors in the company's SEC filings, including our most recent quarterly filings 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, Immune Bio disclaims any obligations to update these forward-looking statements to reflect future information events or circumstances. With that behind us, now I'd like to turn the call over to Dr. RJ Tessie, CEO of Immune Bio. RJ.
spk04: Thank you, David, and thank you, everyone, for joining the call. As usual, I will arrange my remarks to highlight the key takeaways for the third quarter and the subsequent period and include updates on our platform programs. I will start by reviewing our developments of EXPRO before passing it over to Mark Liddell, who will provide an update on IncMUNE. And then David Moss will conclude with a discussion of our financial results and provide an update on upcoming and new milestones. Then we move to Q&A. During the third quarter, our primary focus remained enrollment of patients into ADO2, our blinded randomized phase two trial in patients with early Alzheimer's disease with inflammation, and we focused on increasing our geographic footprint of that trial. We had notable success on both fronts. The MHRA, the UK equivalent of the FDA, approved our clinical trial application in August Five of the six sites in the UK are already screening and enrolling patients into ADO2. The UK is an ideal jurisdiction to expand our Alzheimer's disease trial, given it possesses one of the highest rates of Alzheimer's disease in the Western world, coupled with a robust for-profit medical research infrastructure. Recognition Health, our lead vendor in the UK, has five memory centers with a large Rolodex of clinical trial ready patients. This provides a ready pool of patients to screen for participation in the trial. Recognition Health has a history of enrolling a large number of patients and are incentivized to find the right patients to enroll in our program. Australia, where the trial is furthest advanced, continue to see patients who have completed the six month blinded trial opt in to the phase two open label extension program. We have also submitted regulatory dossiers to additional countries with the plan to have additional sites open soon. This leaves the US and the FDA. The FDA is the outlier here. We remain on track with the FDA to meet the conditions necessary to lift the clinical hold. We believe the hold will be lifted before the end of the year. There are two main themes from the just completed CTAD or Clinical Trials Alzheimer's Disease Meeting in Boston, earlier treatment and better treatments. As you can imagine, we heard a lot about the anti-amyloid therapies. Little new was presented and no matter how they cut the data, there is no change in safety or efficacy of the various anti-amyloid products. Unsurprisingly, a meta-analysis demonstrated all three drugs, aducanumab, lucanumab, and donamimab performed the same. This is shaping up to be an interesting marketing battle debating features, not benefits. In my opinion, the desire for earlier treatments is driven by the frustrating results from anti-amyloid monotherapy. That is, if the results of anti-amyloid drugs were better, there may be less talk about earlier treatment. Both of these themes, the limit efficacy of anti-amyloid drugs in the early treatment, play two ex-pro strengths. The universe of therapies for Alzheimer's disease is expanding. Targeting neuroinflammation is high on everyone's list. Dr. Howard Fillett, the chief scientific officer of the Alzheimer's Drug Discovery Foundation, highlighted the role of inflammation and aging and cognitive decline. In a recent Fierce Biotech interview, Dr. Fillett points out that at autopsy, beta amyloid is present in the brains of many elderly individuals that have died with normal cognitive functions. Only those, and this is the key point, only those with both amyloid and inflammation have dementia. In other words, the immune response to amyloid appears to drive nerve cell death and synaptic dysfunction that results in cognitive decline. His comments highlights our longstanding position. Without inflammation, there is no cognitive decline in patients with amyloid pathology. Combination therapy with the anti-amyloid drugs was much discussed at CTAD, but no data was presented. Once again, the desire for combination therapy reflects a frustration with the current results. Combination therapies, excuse me, must improve safety or efficacy, ideally both. Because the major safety problem with anti-amyloid class of drugs is neuroinflammation, we believe EXPRO plays a role in combination therapy. ImmuneBio has initiated preclinical studies testing combination therapy in animal models. I emphasize the combination therapy is preclinical and in no way dilutes our focus on the phase two trial currently enrolling patients. The discussion on early diagnosis focused on blood tests aiming to produce a simple, accurate, cost-effective triage system. Our view is simple. Cognitive decline is predicted by biomarkers of neuroinflammation and neurodegeneration. Blood amyloid is a biomarker of disease, the disease of Alzheimer's disease. Staging, by staging I mean the severity of the disease, requires a different set of biomarkers. In my opinion, and many of those at the meeting, the most promising duo is GFAP, was glial fibrillary acidic protein, a biomarker of astrocyte activation, and phospho-tau-217, a biomarker of neurodegeneration, are promising. Although we do not use GFAP or p-tau-217 as screening biomarkers for enrollment in the Phase I trial, They were measured as part of the biomarker response package. Both biomarkers decreased in patients after treatment with XPRO. We hope to show that this decrease correlates with clinical response in the Phase II trial. We are persistent in our belief that cognitive decline is the sum of synaptic dysfunction and nerve cell death. Phosphatau is an excellent measure of neurodegeneration, or nerve cell death in patients with Alzheimer's disease, measuring synaptic function is more complicated. A small group of Alzheimer's patients used a self-administered EEG using the novel system from Cumulus Neuroscience. The study confirmed in this small number of patients the feasibility of collecting high-quality EEG signals at home. The patients liked it, and there was evidence of benefit as demonstrated by acute and chronic changes changes in the P300 amplitude on EEG after treatment with EXPRO. Although the group is small and the data are early, we believe this work is further evidence of improved synaptic function after EXPRO treatment. And future work will correlate this activity with cognitive function and pharmacodynamic responses to DN-TNF. This type of home testing may be a key element to CNS drug development in the future. Two other applications of the DNT in a family of drugs are worth mentioning. New data using MbO3 to treat cancer will be presented at the 38th annual Society of Immunotherapy meeting in San Diego later this week. MbO3 has been shown to be an innate immune checkpoint inhibitor that down regulars SIRP-alpha. SIRP-alpha, that is S-I-R-P-alpha, is signal regulatory protein alpha. That is the macrophage side of the CD47 don't eat me signal. Down regulation of SIRP-alpha repolarizes immunosuppressive macrophages in the tumor microenvironment into M2 macrophages that directly kill and phagocytes tumors and improves ADCP, which is antibody-dependent cellular phagocytosis, a key but often ignored effector of anti-cancer antibody therapy. Recent data from the DMD program confirms the potency of the 10 kilodalton PSAR DNTNF in mouse models of the disease. As a reminder, the PSAR DNTNF compounds are the sons of Vexpro with similar biologic activity that allows immune biology to expand applications of the DN-TNF class of compounds beyond CNS. The goal of the MBO3 cancer program and the DMD program is to out-license these promising drugs. Some of you are wondering how a single drug, dominant negative TNF inhibitors, can be useful in the treatment of cancer and the treatment of Alzheimer's disease. Macrophage function is the glue that holds this story together. Microglia are tissue-based macrophages of the brain. TAMs, or tumor-activated macrophages, are tissue-based macrophages in the TME of cancer. In disease, chronic inflammation, shall we say, stuns the macrophages into not working. In the brain, chronic neuroinflammation causes the microglia to become dysfunctional, a dysfunctional phenotype that produces destructive cytokine, does not phagocytize cellular and myelin debris, and does not prune synapses appropriately. This results in nerve cell loss, demyelination, and synaptic dysfunction, the hallmarks of neurodegenerative disease, including Alzheimer's. DN-TNF converts the destructive microglia into a reparative cell type that promotes nerve cell survival, remyelination, and synaptic classivity. The remodeling and repair we have seen in the brains of patients with Alzheimer's disease treated with Expro reflect the normalization of microglial function caused by Expro. In cancer, soluble TNF produced by tumor cells causes expression of MUC4, SERP-alpha, and other immunosuppressive cytokines that polarize TAMs to an immunosuppressive phenotype that promotes and protects tumor growth and metastasis. These elements also promote resistance to immunotherapy. EXPRO neutralizes soluble TNF resulting in M2 macrophages that do not express SERP-alpha, kill tumor cells, promote ADCP. On the tumor, EXPRO down-regulates MUX4 to expose the tumor to immune attack. In summary, ExPRO improves the function of innate immune cells needed to defeat the ravages of neurodegenerative diseases of the brain and cancer, and the macrophage is the common denominator to these effects. I will now pass this to Mark Liddell, the founder and CSO of ImmuneVial, to update the progress on the InCMU program. Mark.
spk00: Thank you very much, RJ. And once again, I'd like to pass my thanks to those that are listening in and joining this third quarter report. So as you know from the last quarter report, we filed an IND with the FDA in April this year for a U.S. trial of INCMUNE in metastatic castration-resistant prostate cancer. We received subsequent clearance in May for the use of INCMUNE in a Phase I, Phase II open-label trial across multiple U.S. centers. And the response since then from potential clinical sites has really been overwhelming. We have eight sites already selected to participate in the trial. The first two sites will be initiated within two weeks time in November, meaning that we're ahead of schedule for the planned first patient treatment before the end of the year. The other sites will come online in the first quarter of 2024. Most importantly, the batch of IncMune has already been manufactured for the treatment of the first U.S. cohort and is just about to be shipped to Amplify Bio, the U.S. distribution center. Patients at each dose level will receive all three doses of IncMune as an outpatient treatment during the six-month trial, and this is really critical to our future development of the drug. Two types of IncMune efficacy will be measured, immunological efficiency and therapeutic efficacy. Immunologic efficacy will measure the increase in these memory-like NK cells that INCMUNE generates in the blood of the patient and how long those cells remain in the patient's blood after treatment, just as we have done in the MDS patients in the Laurel trial. Therapeutic efficacy will measure tumor response to INCMUNE therapy using biomarkers of prostate cancer tumor burden, such as changes in blood PSA level, PMSA scan, and circulating tumor DNA. In addition, traditional measures of disease progression will be measured, including progression-free survival, changes in resist criteria using CT scan and bone scan. But as you might imagine, these are not expected to change in such a short six-month study. In the UK and Europe, we've managed to advance the Laurel trial in MDS and AML. I'm sure you've shared with us the extreme frustration in the lack of recruitment in the UK. to that trial. And this has been due to the changes in the clinical management of these patients in the UK in the new, what we like to call post-COVID era. But as a man who got COVID for the first time in August, we're planning not post-COVID. At a meeting of the Trial Safety Committee held earlier this year, the enrollment safety criteria was modified in an attempt to limit screening failures. A protocol amendment was submitted to the MHRA back in May and finally was approved last week. So we've submitted the revised protocols to the two UK clinical sites for immediate initiation, and the largest cancer center in the UK, the Royal Marsden Hospital, has just come online and will be initiated soon. Meanwhile, the complexities of importing IncMune into Greece for the Greek trial and establishing local laboratory monitoring of patients have all been resolved over the summer, and the first batch of drug is ready to be delivered to the hospital in Athens. A patient has completed screening and is going to be reviewed on the 3rd of November for determination, finally, of suitability for inclusion. and treatment, so we hope to close the first cohort with that patient. We remain very excited about the potential of IncMune platform as it begins its transition into the treatment of solid tumors. And I remind you, those are the tumors that account for approximately 90% of human cancer. For reasons we understand, most cell therapies currently focus on that 10% of cancers that are hematological tumors. But our confidence in the use of IncMune in solid tumors is based on good biology. In vitro data in solid tumors from my lab shows that IncMune arms natural killer cells to override the immunosuppression of hypoxia and regulatory cells in the tumor microenvironment of solid tumors. The company presented the data on the IncMune-driven memory-like NK cells in the presidential symposium at the annual conference of the International Society of Cell and Gene Therapy in June, and we continue to follow up those data to study IncMune effect on NK cells at the molecular level. You'll hear more on this in the future. In my previous role as director of the cell and gene therapy facility at the Royal Free Hospital and University College London, I spent over 30 years producing cell therapies for academic and small spin-out company clinical trials. When these therapies attempted to enter the commercial world, many failed due to manufacturing issues. As I'm sure you know from the CAR-T story, manufacturing of cell therapies is difficult to do at scale. But we've solved that problem with a robust and scalable process for INCNEW. We've been successful in upscaling the manufacturing process and have completed the validation of that new process to CGMP. We've since signed a contract with a commercial contract manufacturing site, and the installation of equipment for that site has now started. So we're ready to move out into a commercial manufacturing setting. This investment paves the way for ambitious plans for trials in other solid tumors, including ovarian, renal and nasopharyngeal cancer as we acquire more and more and more of the relevant supporting data. The company remains committed to execute on its vision of moving Incmune forward towards commercialization. That ends my update on the Incmune platform, and I'd like to turn the call over to David Moss, CFO, to discuss the financials. Thank you, David.
spk02: Super. Thank you, Mark. I'll provide a brief overview of our financial results and upcoming milestones before we head to the Q&A session. Net loss attributable to common stockholders for the quarter ended September 30th, 2023 was approximately 8.6 million compared with approximately 7.7 million for the comparable period in 22. Research and development expense totaled approximately 6 million for the quarter ended September 30th, 23 compared with approximately 5.2 million for the comparable period in 22. General and administrative expense was approximately 2.6 million for the quarter ended September 30th, 2023 compared with approximately $2.4 million for the comparable period in 2022. At September 30, 2023, the company had cash and cash equivalents of approximately $41.8 million. Based on our current operating plan, we believe cash is sufficient to fund our operations until late 2024. As of November 1, 2023, the company had approximately 18 million shares of common stock outstanding. As highlighted in the prior quarters investor call, we continue to focus on achieving our primary clinical trial objectives or remaining cost prudent with the potential to recover a portion of R&D expenses in Australia and in the UK. Now I'd like to move on to our list of upcoming and important milestones. First milestone that we have, which we hope to have before year end, is the removal of the FDA hold. We expect top-line results from our Phase II early AD program towards the end of 2024. Upon release of the FDA hold, we'll initiate a Phase II trial of XPRO in patients with treatment-resistant depression. Additional open-label Phase I data of ink moon in high-risk MDS and AML in 2024 and the initiation of a phase one slash two program in metastatic castration-resistant prostate cancer with the first patient treated before year end and open label data in 2024. We expect an upcoming webinar on the use of Expro to promote remyelination in neurodegenerative disease. And finally, wearing my business development hat for a moment, the DMD market with inconsistent results in gene therapy and confirmatory trials for exoscoping drugs still long underway is confusing. We feel that Expro could be a novel solution to replace corticosteroids in DMD. Corticosteroids, including one approved last week, target the same glucocorticoid receptor pathway and have the same immunologic, metabolic, and cosmetic side effects and paradoxically cause muscle atrophy. Targeting soluble TNF with DN-TNF prevents inflammation and muscle degeneration and promotes muscle regeneration in animal models without evidence of off-target safety issues seen with the use of corticosteroids or non-selective TNF inhibitors. Interestingly, TNF is overexpressed in DMD at early stages of the disease where inflammation induces muscle degradation. Because corticosteroids are the most common drug used to treat DMD, a strategy that provides the benefit of corticosteroids without the side effects will benefit all patients with DMD regardless of age, stage of disease, or concomitant therapy. This is what excites us about the DN-TNF platform for DMD. As always, I think our shareholders understand that we continue to pursue business development partnership opportunities for DNTNF in DMD and potentially other applications, but there can be no assurance that the company can complete any of these transactions as they're complex and difficult. In summary, management feels that the company has two great platforms, and as a small organization with limited resources, we will try to expand the applications of these platforms in order to benefit shareholders. Naturally, we'll update investors should material business development events occur. At this point, I'd like to thank you for your time and attention. I'd like to turn it back to Claudia to poll for questions. Claudia?
spk01: Thank you very much, sir. At this time, we will be conducting a question and answer session. If you'd like to ask a question, please press star and then one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star and then two if you would like to remove your question from the queue. Please limit your questions to one question and one follow-up question. For participants using speaker equipment, it may be necessary for you to pick up your handset before pressing the star keys.
spk07: One moment please while we poll for questions. The first question comes from Joel Beattie from BIRD.
spk01: Please proceed with your question, Joel.
spk06: Hi. Thanks for taking the questions and congrats on the progress. My first question is on ExPRO. Could you discuss a little bit more about what gives you confidence that the clinical hold will be lifted by the end of the year?
spk04: Yeah. Thank you, Joel. RJ here. Although it took a while to get to an agreement with the FDA, as I think I highlighted at the last call, they gave us a list of things they wanted done. Um, obviously those are those, that list was different than any of the other regulatory agencies. And we have gone through that list and the data is, you know, uh, been completed. It is being packaged and will be sent to the FDA for, to meet the, uh, the goal to have us off hold by the end of the year. I, you know, they, they, ultimately gave us quite a clear list, and we have fulfilled it.
spk06: Great. And then as a follow-up for the ADO2 study in early Alzheimer's, are you able to provide any more information on where you're at in enrollment or what the approximate geographic split could end up looking like?
spk04: Yeah, I think, you know, we mentioned this last time. We're We're changing our geography so quickly that we've been reluctant to really give names, numbers and names yet. I think later, early in 2024, when things have kind of settled down, I guess that's the way to describe it, we'll be able to give clear direction on where we are. outside of uh as far as clinical sites how many sites are involved but i would be willing to bet there'll be more than 50 sites open by the end of this process uh i won't promise that any will be in the u.s because we're really expanding so quick quickly outside of the u.s but as we said last time you know this is really setting us up for the phase three trial i mean it's global multiple continents and I know this has been a very frustrating but the one thing we are careful about is we don't want to when we give you information we want it to be perfect in other words we want to be able to back it up and things are just changing so quickly and quite frankly to our advantage and I think the UK is a good example we have we're ahead of where we expected to be in the UK. They had a great backlog of patients that hopefully will all be screened and many of those will end up in the trial. So all I can say is you all hang tough. And, you know, I think right now we have not changed our guidance. We still expect to be able to provide top lane data by the end of the 2024. And I can tell you that everyone in this company is busting a gut to get us there.
spk08: That sounds great. Thank you.
spk01: Thank you. The next question comes from Tom Schrader from BTIG. Please proceed with your question, Tom.
spk03: Good afternoon. Thanks for holding the call. We enjoyed your CTAD presentations. Just to follow up on Joel's line of questioning, the late 24 data, could that be done with no U.S. participation or are they linked?
spk04: So, yeah, it could be done. We're driving forward, Tom. And, by the way, Tom, this is RJ. Thank you for the question. No, it could be done without U.S. participation. I mean, you know, remember from the time – let me use the prostate cancer trial that we're running as a great example. You know, Mark said we got the green light in, I believe it was May – And we didn't do any front-loading planning there because that's expensive. And as you know, we're careful with our money. So from the time we got the green light to the time we're going to get our first patient enrolled will be six to seven months, right? That's just what it takes if you go from a standing start, right? So in the U.S., that's what will happen. Once we get off hold, we'll start casting the U.S. net, right? But by the time those sites get ready to go, we may have enrolled the trial. Now, there's a lot of other things we can do. We don't want to frustrate clinical sites. But I couldn't, I think I've said it before. Maybe I've just said it privately. You know, one of the things that frustrates us is that, you know, clearly what the FDA is doing is different from what the other regulatory agencies are doing. All these other countries, their patients are getting access to what we think is a pretty good drug, expo for Alzheimer's disease. The U.S. patients are sitting on the sideline because of a regulatory challenges, but with the FDA. I can promise you the U.S. will be involved in the phase three trial and will probably be the main driver of the phase three trial. But I wouldn't be surprised if we complete the phase two trial without U.S. patients.
spk03: Got it. And if I can follow up, given we have Mark on the line. Mark, in the Incommune Prostate Cancer Trial, who are these patients? Are they post-taxing? And I guess, is the trial monotherapy? And then the final question is, you know, the oncology world has bent over backwards to try to get prostate cancer to be an immunoreactive tumor that, you know, Xtandi and Nevo went on for years, and now it's Nevo, Ipi, and Do you see IncMune playing there that it might be the final piece to make prostate cancer NEVO reactive? Is that interesting to you, or is this pretty much a monotherapy endeavor for at least a while?
spk00: That's a really, really excellent question, and I would love to spend a long time on slides and put my academic hat on. I think the first question, yes, these are going to be post-taxane patients. They're end-stage patients because that's what you always do in a phase one trial. But the question about failure of the checkpoint inhibitors, every immunotherapy that's been tried in prostate so far has targeted T cell responses. And the immunosuppressive microenvironment of the tumor is high. And whether that be checkpoint inhibitors or whether it be antibody conjugates, they've failed. If you read the literature and if you go and speak to a histopathologist, they'll tell you that if you look at patients who do well in conventional therapy in prostate cancer, They're patients who have a large NK cell infiltrate in their tumor. There isn't an association with a T cell infiltrate. So what we're targeting in the cells are already in the tumor. We're just trying to switch them on to be better, like we are in AML and MDS. And we know that there's a dirty little secret about solid tumors is this thing called neutrophil extracellular traps that coat the tumor. And they inhibit NK cell activity. It means the NK cells and the T cells can't get to the tumor. Well, we're targeting... tumor infiltrating NK cells that are already there. So that overcomes part of that problem. But the really interesting thing about these neutrophil and extracellular traps that stop particularly T cells invading from the peripheral blood is that they are broken down by M2 macrophages. So one of the great things that might come out of the EXPRO trial is that, or IMD03, is that you could actually combine those two drugs in a very, very nice way to break down the traps, to enhance the T cell entry into the tumor, and then respond to the initial response that's generated by the NK cells that are there. So I think that's a really exciting combination trial that I'd love to do. That could also be combined with a conventional T cell checkpoint inhibitor, because once the T cells are there, you want to make certain they're not inhibited further by by the inhibitory checkpoints in the tumor. So yes, I'd love to think further down the line, we would look at combination therapy. The immune system never works on a single cell. There's never been a single approach that's worked. So it'd be really, really nice to think that we could provide a long-term benefit by combining these.
spk08: Great. Thank you.
spk01: Thank you. Ladies and gentlemen, just another reminder, if you'd like to ask a question, please press star and then one. If you'd like to ask a question, please press star and then one. The next question comes from Daniel Carlson from Tailwinds Research. Please proceed with your question, Daniel.
spk05: Hey, guys. Just a couple of follow-up questions here. Regarding IncMune, I just saw that Amgen pulled a drug from clinical trials yesterday and prostate and wrote down about $600 million. I was wondering if you could comment on how that impacts your thinking about your program at all, if at all.
spk00: Yeah, if I have a stab at that, I think much as I said just now, I don't think T cells immediately are the answer in prostate cancer. And the anti-CD47 antibody you're talking about is a good example of that. The checkpoint inhibitors haven't worked. The anti-CD3 combination antibodies haven't worked. So I think we need to look at, excuse me, we need to look at activating the cells that are actually there. And so it just makes me more enthusiastic about the prospects.
spk05: Great. That's what I thought. Thanks, Mark. And then a question about Sarepta missed their top line yesterday as well. I know they're the leader in DMD. Is this something that you think might push them towards working with you guys, or how do you see that all unfolding at Sarepta?
spk09: David?
spk02: You know, you're asking me to guess what Sarepta is going on. I can tell you they're going through probably a pipeline reorganization process. You know, I think that you recently had a steroid that was approved that's supposed to be a slightly better steroid than the current standard of care. As I spoke about earlier, you know, we believe that EXPRO going down a completely different pathway than what steroids pathway provides significant benefit over a lot of the problems that are associated with steroids. You know, DMD is really an interesting space because You know, the exon skipping drugs all have confirmation trials, which are still ongoing. They're kind of a long, they've been taking a long time while they keep these drugs on the market. It's going to be interesting to see what the FDA does with the fact that the confirmation trial for the gene therapy that Sraptoran is, you know, failed. And, you know, there's some thought on the street that they keep the program on the market. I don't know what's going to happen. My guess is with what the FDA has done with regard to that program have been wrong. So I wouldn't hold any of that water. But, you know, bottom line is that we feel that there needs to be a new approach to DMD beyond exon skipping, beyond steroids, and beyond gene therapy. And we think that DN-TNF is a really great approach. We like it a lot.
spk08: Thanks, David.
spk05: That's it for me, guys.
spk08: All my other questions were asked already, so thank you.
spk01: Thank you very much. Ladies and gentlemen, we have reached the end of the question and answer session, and I'd like to turn the call back to RJ for closing remarks. Thank you, sir.
spk04: Sure, thank you. Immune Bio is making progress on two fronts. Each of our platforms have had a significant increase in shall we say, profile in the last quarter. With EXPRO, we hope to have a therapy that stops the progression of cognitive decline in patients with ADI, with Alzheimer's disease. That's very different than what is offered patients today. With INCMUNE and metastatic castrate-resistant prostate cancer, we hope to control a disease that in many men can be quiet and indolent, but in many is lethal. We are confident in these ambitious goals. We thank you for your attention today, and to those of you that are shareholders, we thank you for your continuing support. With that, have a good day.
spk01: Thank you. This concludes today's conference. You may disconnect your lines at this time, and thank you very much for your participation.
Disclaimer