INmune Bio Inc. (INMB) Earnings Call Transcript & Summary

Greetings, and welcome to the INmune Bio Third Quarter 2023 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, CFO of INmune Bio. David, the floor is yours.

Thank you, Claudia, and good afternoon, everybody. We thank you for joining us for the -- for INmune Bio's Third Quarter 2023 financial results. With me on the call is Dr. RJ Tesi, CEO of INmune Bio, and Dr. Mark Lowdell, Chief Scientific Officer of INmune Bio who'll provide an update on INKmune, our memory-like natural killer cell oncology platform. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release as well as risk factors in the company's SEC filings, including our most recent quarterly filings 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, INmune 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 Tesi, CEO of INmune Bio. RJ?

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 XPro before passing it over to Mark Lowdell, who will provide an update on INKmune. 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 in the AD02, our blinded randomized Phase II 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 U.K. equivalent of the FDA, approved our clinical trial application in August. Five of the 6 sites in the U.K. are already screening and enrolling patients into AD02. The U.K. 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 U.K., has 5 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 was furthest advanced, continue to see patients who have completed the 6-month blinded trial and opts in to the Phase II 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 U.S. 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 2 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 3 drugs, aducanumab, lecanemab and donanemab 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 to XPro strengths. The universe of therapies for Alzheimer's disease is expanding, targeting neuroinflammation is high on everyone's list. Dr. Howard Fillit, 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. Fillit points out that at autopsy, beta-amyloid is present in the brains of many and elderly individuals that have died with normal cognitive function. Only those, and this is the key point, only those with both amyloid and inflammation, have dementia. And 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 long-standing 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 refrustration with the current results. Combination therapies must improve safety or efficacy ideally both. Because the major safety problem with anti-amyloid class of drugs is neuroinflammation, we believe XPro plays a role in combination therapy. INmune Bio has initiated preclinical studies, testing combination therapy in amyloid -- in animal models. I emphasize the combination therapy is preclinical and in no way dilutes our focus on the Phase II trial currently enrolling patients. The discussion on early diagnosis focused on blood test 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. Phospho-tau 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 the 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 [ cutanchron ] exchanges -- changes in the P300 amplitude on EEG after treatment with XPro. While the group is small and the data are early, we believe this work is further evidence of improved and synaptic function after XPro 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 DN-TNF family of drugs are worth mentioning. New data using INB03 to treat cancer will be presented at the 30th -- 38th Annual Society of Immunotherapy meeting in San Diego later this week. INB03 has been shown to be an innate immune checkpoint inhibitor that down regulars SIRPalpha. SIRPalpha that is S-I-R-P alpha is signal regulatory protein alpha. That is a macrophage side of the CD47 don't eat me signal. Down regulation of SIRPalpha repolarizes immunosuppressive macrophages in the tumor microenvironment into M2 macrophages that directly kill and phagocized tumors and improves ADCP, which is antibody-dependent cellular phagocytosis, a key but often ignored factor of anticancer antibody therapy. Recent data from the DND program confirms the potency of the 10-kilodom PSAR, DN-TNF in mouse models of the disease. As a reminder, the PSAR DN-TNF compounds are the sons of XPro with similar biologic activity that allows immune bio to expand applications to the DN-TNF class of compounds beyond CNS. The goal of the INB03 cancer program and the DMD program is to out-license these promising drugs. Summary, 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 a dysfunctional phenotype that produces destructive cytokine does not phagocytize cellular and myelin debris and does not prune synapsis appropriately. This results in nerve cell loss, demyelination and synaptic dysfunction, the hallmarks of neurodegenerative disease, including Alzheimer's. DN-TNF converts the destructive microglial phenotype into a reparative cell type that promotes nerve cell survival demyelination synaptic plasticity. The remodeling and repair we have seen in the brains of patients with Alzheimer's disease treated with XPro, reflect the normalization of microglial function caused by XPro. In cancer, soluble TNF produced by tumor cells causes expression of MUC4, SIRP-alpha and other immunosuppressive cytokines that polarized TAMs to an immunosuppressive phenotype that promotes and protects tumor growth and metastasis. These elements promote -- also promote resistance to immunotherapy. XPro neutralize soluble TNF resulting in M2 macrophages that do not express SIRP-alpha TIL tumor cells promote ADCP. On the tumor, XPro down regulates MUC4 to expose the tumor to immune attack. In summary, XPro improves the function of innate immune cells needed to feat 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 Lowdell, the Founder and CSO of INmune Bio, to update the progress on the INKmune program. Mark?

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 INKmune in metastatic castration-resistant prostate cancer. We received subsequent clearance in May for the use of INKmune 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 8 sites already selected to participate in the trial. The first 2 sites will be initiated within 2 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 INKmune 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 3 doses of INKmune as an outpatient treatment during the 6-month trial, and this is really critical to our future development of the drug. Two types of INKmune efficacy will be measured, immunological efficiency and therapeutic efficacy. In immunologic efficacy will measure the increase in these memory-like NK cells that INKmune 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 RARA trial. Therapeutic efficacy will measure tumor response to INKmune 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 RECIST criteria using CT scan and bone scan. But as you might imagine, these are not expected to change in such a short 6-month study. In the U.K. and Europe, we've managed to advance the Laurel trial in MDS and AML. I'm sure you would be -- you've shared us -- with us the extreme frustration in the lack of recruitment in the U.K. to that trial. And this has been due to the changes in the clinical management of these patients in the U.K. 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 now 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 filing was approved last week. So we've submitted the revised protocols to the 2 U.K. clinical sites for immediate initiation and the largest cancer center in the U.K., the Royal Marsden Hospital has just come online and will be initiated soon. Meanwhile, the complexities of importing INKmune 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 third 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 INKmune 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 INKmune in solid tumors is based on good biology. In vitro data in solid tumors from my lab shows that immune arms natural killer cells to override the immunosuppression of hypoxia and regulatory cells in the solid -- in the tumor microenvironment of solid tumors. The company presented the data on the immune-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 INKmune factor in 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 INKmune. We've been successful in upscaling the manufacturing process and have computed -- 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 our 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 INKmune forward towards commercialization. That ends my update on the INKmune platform, and I'd like to turn the call over to David Moss, CFO, to discuss the financials. Thank you, David.

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 30, 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 30, '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 30, 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 into late '24. As of November 1, '23, the company had approximately 18 million shares of common stock outstanding. As highlighted in the prior quarter's 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 U.K. Now I'd like to move on to our list of upcoming and important milestones. First milestone that we have, which is we hope to have before year-end is the removal of the FDA hold. Second, 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 INKmune in high-risk MDS and AML in 2024 and the initiation of a Phase I/II 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 XPro to prevent 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 access skipping drugs still long underway is confusing. We feel that XPro could be a novel solution to replace corticosteroids in DMD. Corticosteroids, including one approved last week, target the same glutacorticoid, 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 nonselective 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 DN-TNF in DMD and potentially other applications but there can be no assurance that the company can complete any of these transactions as they are complex and difficult. In summary, management feels that the company has 2 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. Natural will 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?

[Operator Instructions] The first question comes from Joel Beatty from Baird.

Congrats on the progress. My first question is on XPro. Can you discuss a little bit more about what gives you confidence that the clinical hold will be lifted by the end of the year?

Yes. 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. 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 has been completed. It is being packaged and will be sent to the FDA for -- to meet the goal to have a soft hold by the end of the year, right? They ultimately gave us quite a clear list and we have fulfilled it.

Great. And then as a follow-up, for the AD02 study in early Alzheimer's. Are you able to provide any more information on where you're in enrollment? Or what the approximate geographic split could end up looking like?

Yes. I think we mentioned this last time, we're changing our geographies 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 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. I won't promise that any will be in the U.S. because we're really expanding so quickly outside of the U.S. But as we said last time, this is really setting us up for the Phase III trial. I mean it's global multiple continents. And I know this has been a very frustrated. 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 U.K. is a good example. We have -- we're ahead of where we expected to be in the U.K. 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, Joel, hang tough. And I think right now, we have not changed our guidance. We still expect to be able to provide top line data by the end of the 2024. And I can tell you that everyone in this company is busting the guts to get us there.

The next question comes from Tom Shrader from BTIG.

Thanks for holding the call. We enjoyed your CT 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?

So yes, 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 remember from the time -- let me give you -- let me use the prostate cancer trial that we're running as a great example. Mark said we got the green light and I believe it was May. And we didn't do any front load. Front load we've been 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, so the time we're going to get our first enrolled -- patient enrolled will be 6 to 7 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. If we -- once we get off hold, we'll start casting the U.S. net. 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, one of the things that frustrates us is that clearly, what the FDA is doing is different from what are the other regulatory agencies are doing. All these other countries, their patients are getting access to what we think is a pretty good drug, XPro for Alzheimer's disease. The U.S. patients are sitting on the sidelines because of regulatory challenges, both with the FDA. I can promise you the U.S. will be involved in the Phase III trial and will probably be the main driver of the Phase III trial. But I wouldn't be surprised if we complete the Phase II trial without U.S. patients.

Got it. And if I can follow up, given we have Mark on the line. Mark, in the INKmune prostate cancer trial, who are these patients? Are they post-taxane? And I guess, is the trial monotherapy? And then the final question is the oncology world has bent over backwards to try to get prostate cancer to be an immunoreactive tumor that XTANDI and nivo went on for years and now it's nivo, ipi. And do you see INKmune playing there that it might be the final piece to make prostate cancer nivo reactive? Is that interesting to you? Or is this pretty much a monotherapy endeavor for at least a while.

That's a really, really excellent question, and I would love to spend a long term slides and put my academic hat on. So I think the first question, yes, these are the post-taxane patients. They're end-stage patients because that's what you're always doing getting to Phase I 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 even suppressive microenvironment of the tumor is high. And whether that be checkpoint inhibitors or whether it be antibody conjugates, they failed. If you look -- if you read the literature and if you go and speak to a histopathologist, they'll tell you that very few -- if you look at patients who do well in conventional therapy in prostate cancer, there are patients who have a large NK cell infiltrate in their tumor. There isn't an association with the 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 to tell a 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 new extracellular traps that stop particularly T cells invading from the peripheral blood is that they are broken down by macrophages. So one of the great things that might come out of the XPro trial is that, I believe there are 3 is that you could actually combine those 2 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 is 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 checkpoint -- conventional T cell checkpoint inhibitor because once the T cells are there, you want to make certain they're not inhibited further 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 works. So it would be really, really nice to think that we could provide long-term benefit by combining these.

[Operator Instructions] The next question comes from Daniel Carlson from Tailwinds Research.

Just a couple of follow-up questions here. Regarding INKmune, and 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?

Yes. 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 for INKmune.

Great. That's what I thought -- and then a question about Sarepta missed their top line yesterday as well. I know they are the leader of 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?

David?

You're asking me to guess what Sarepta is going on. I can tell you they're going through probably a pipeline reorganization. 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, we believe that XPro going down a completely different pathway than where steroids -- than what steroids pathway provides significant benefit over a lot of the problems that are associated with steroids. DMD is really an interesting space because 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 Sarepta is failed. And 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 won't hold any of that water. But the bottom line is, 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.

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.

So thank you. INmune Bio is making progress on 2 fronts. Each of our platforms have had a significant increase in, shall we say, profile than the last quarter. With XPro, we hope to have a therapy that stops the progression of cognitive decline patients with ADI with Alzheimer's disease. That's very different than what is offered patients today. With INKmune and metastatic castrate-resistant prostate cancer, we hope to control a disease that many men can be quiet in 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.

Thank you. This concludes today's conference. You may disconnect your lines at this time, and thank you very much for your participation.