Date and answer questions fr om the audience. Before we begin, I would like to remind everyone that today's call may include forward-looking statements. These statements are based on current expectations and assumptions and are subject to risks and uncertainties that could cause actual results to differ materially from those projected. For more information on the risks and uncertainties related to Annovis Bio's business, please refer to the forward-looking statements and the company's latest SEC filings. To guide us through today's presentation, I am pleased to introduce our speaker, Dr. Maria Maccecchini, the founder, President, and CEO of Annovis Bio. Today's presentation will address the current progress of Alzheimer's and Parkinson's clinical programs, including the pivotal phase III Alzheimer's trial, the upcoming open label extension for AD, and the ongoing open label extension for PD. The presentation will also cover clinical and corporate milestones anticipated in the coming months. During the webcast, we welcome our audience to leave a question in the comments section, the Q&A box, or raise hand by using a button in the task bar. Once it's your turn, you'll be unmuted and allowed to ask your question directly. Now without further ado, I will turn the call over to Dr. Maria Maccecchini. So all over to you, Dr. Maria. Good afternoon, and thanks a lot for joining us. This is a really good time in our life because it feels like we are almost there. Let me tell you what almost there means. We have 42 million outstanding shares, and we are the only company that has a drug that works in Alzheimer's and Parkinson's. We still have $19 million in the bank, so we're not totally desperate, and we are in late-stage development. The most important thing that we're going to be discussing today is that we have the pivotal phase III Alzheimer data read out in March. It's coming up. The pipeline hasn't changed a lot other than we have added open label studies to Alzheimer's and to Parkinson's disease. In terms of the combination, some of you sometimes ask me, we really don't have money to do that. What we are doing is additional combinations in mice to figure out why these combinations work and to better understand the brain. Because if we can better understand the brain, we can actually treat it better. This is our patent portfolio. I told you we are working on combinations, and if you look at the very top, you have cancer combinations, statin combinations, and how our drug works with all these other drugs. This right now is more in the research stage, but we are publishing, and we are obviously filing patents. I wanted to spend a minute talking about our people. I usually just say we are a young, aggressive, very hardworking team. We are. But I do want to point out that while we are small, we are doing a really fantastic job. Cheng Fang is our Chief Scientific Officer. She is probably the most innovative person in the world in terms of biomarkers, not because other people don't know more, somebody may know more, but because she's really actually using them in our studies, and that is unusual. Most people don't measure half the biomarkers she does. She is also really fantastic in designing our studies. We have heard from a number of PIs and KOLs that our studies are fantastic. Eve has been running our regulatory group for over 15, 16 years. While she seems alone here, she actually has nine people reporting to her, and she has touched every single aspect of regulatory. We just started filing the NDA. We started putting in the modules for the NDA, so we will be ready next year to file it. Sarah is a fantastic organizer. She is running clinical studies. She is running three CROs and over 50 people. We could never do this study without her. Mike, well, he is doing three large batches. He has run our CMC since inception. Our drug is 99.999% pure, and we are at the registration batch study. Hui Liu is running statistics together with three other groups. So again, she has a lot of people. I want to point out Alex, who is our do everything boy. He wrote the history of buntanetap. If you haven't read it, you should really read it. He just wrote a paper on AI and how Alzheimer drugs go into the brain. Alex is also our Director of Strategic Communication. As I said, he is very multifaceted. He's setting up our AI in-house. While you see these people here, behind this group, we have over 30 people. I've told you before several times that our drug inhibits more than one neurotoxic aggregated protein. It does. Because it does, it can be used in Alzheimer's and in Parkinson's disease. I've also told you that in order to develop a drug, it takes more than one study. It takes an enormous amount of studies. In fact, we have treated to date over 1,600 patients. We have finished 13 studies and are in two large studies. One is the pivotal Alzheimer's study we are talking about, one is the open label Parkinson's. Altogether, we will end up with maybe 1,700 or 1,800 patients by the time we file the NDA. Let's go to the study everybody wants to know everything about. You know we're fully enrolled. We enrolled much better than expected. At the end of the year, so December 31st, is the last person last visit for the six month study. Then we have to clean the data, lock the data, analyze the data, and in March of 2027, we will present at ADPD. The data, we don't have a choice. Since all this is organized, in March, we will present the top-line data. That data, the six months data, filing an NDA at that point, puts us into a $7 billion generic market. That market consists of Aricept, Namenda, and Exelon. As I said, it's a 30-year-old market, it's generic, and in spite of that, just in the U.S., we're selling $7 billion worth of drug. Study will continue for an additional 12 months, and then in March of 2028, we will have the top-line data for the 18 month, disease-modifying readout. Now, that market is estimated to be $100 billion, and we do want to be part of that market. How does the statistics for this study look to date? The study was started in January of 2025, and I'm giving you data up to July of 2026. Last year, in 12 months, we recruited 200 patients. That was slow. We really sped up, and this year we recruited 662 patients until the end of July. The screen failure rate is 67%. That compares favorably to the existing anti-amyloid drugs like Leqembi, Kisunla, and aducanumab. They had a 70%-80% screen failure rate. So we are a little better, but not much. The dropout rate, however, is fantastic. We only have an 8% dropout rate. If we compare that to the amyloid drugs, they have a 20%-30% dropout rate. And we have no drug-related serious adverse events. This is good statistics. If we keep this 8% dropout rate, we will actually finish the study with about 790 patients, which is plenty. Maybe a little bit more detail about the study we are doing now. We had very stringent inclusion criteria. Just like in our previous studies, we first relied on the PI's analysis of does this person have Alzheimer's or not? However, we also measured the MMSE. It had to be over 20 and below 29. We measured p-tau to make sure they had Alzheimer pathology. And we did MRI, A, to see whether the brain was healthy, but B, also to give a baseline as to the volume of the brain. The primary endpoints for both the six and the 18 months are ADAS-Cog 13 and ADCS-ADL. That is exactly what the FDA asked us to do. This is exactly what we do. At 18 months, we have added secondary endpoints, volumetric MRI and p-tau217, to show disease modification. And then we will do biomarkers. And we have seen in biomarkers in a number of studies, that I'll show you a little later, that our drug consistently lowers inflammation. And that is very important because you do not want to have inflammation in your brain independent of what disease you have. The planned open label, which will continue once the patients have reached 18 months. We don't expect that many patients because an 18-month study is a long study, and adding to that two years is really long for the patients to be continuously monitored. But we open it up to whoever wants to. Now, from an FDA point of view, an open label study really only counts for safety. However, for us, we can see how the patients that were on placebo do once they come off placebo and go on drug, how the patients that have been on drug progress or stay the same. And so the open label will give us indication on whether the disease continues to go downhill or stays the same, and how it differs from the patients that were on placebo and the patients that were on drug. And now I'm taking a step back because I told you what study we are doing. But why are we so sure that the study we are doing actually is going to work? The reason we are so sure that the study we are doing is actually going to work is because we are basing it on the previous study that unfortunately only worked in a subgroup. In the previous study, we were not half as selective in how we put people into the study. We relied on the PI to tell us whether the person had Alzheimer's. It turns out a lot of patients didn't. We didn't do p-tau. We didn't do MRI. Our MMSE was too advanced. The endpoints per se were correct. There was nothing wrong with them. In that study, we did look at three doses, and of course, we had placebo. The ITT, intent to treat population, did not show statistical improvement in cognition. However, when we then took a subgroup that consisted of p-tau217 positive patients, which are patients that actually had amyloid in the brain and were confirmed to have Alzheimer's disease, and we looked at the three doses, we saw that 30 mg, the pink bar, is by far the best. The study we are doing now are the patients that are identical to the patients in this pink bar. If we look at the patients in the pink bar, we don't just see that they improved in cognition, but they improved in inflammation. They improved in five different inflammatory factors, and they improved in neurofilament light. The reason I'm highlighting neurofilament light is that the FDA has approved neurofilament light as a biomarker for ALS. Actually, if you show an improvement in neurofilament light in ALS, you get approval. ALS is an orphan indication, and of course, the FDA is not going to approve neurofilament light for Alzheimer's disease. But the fact that the FDA believes in neurofilament light and the fact that we are reducing it, and I'm just showing you here in one population, we have actually reduced neurofilament light in every population we ever treated. That means that we are pretty sure that our nerve cells are healthier than the ones of patients that were not treated. Let's move to Parkinson's disease. In Parkinson's disease, we have an open-label study. We have enrolled something like 280 and 85 patients. It is a 36-month study, but it's not because it's 36 months, it's because we want to keep patients or give patients the opportunity to stay on the drug until the drug is on the market. The protocol was approved. The interesting thing about this study is that we are measuring a lot of things. The reason we are measuring a lot of things, this is an opportunity for us to understand Parkinson's disease. We didn't measure much in our previous study, so we're measuring it here. We also are planning a Parkinson's disease dementia study because exactly like in Alzheimer's, we found a subgroup that reacted very well to our drug. Let's go and show you the design of the open label for Parkinson's disease. It's really quite simple. For patients that have been on the drug before, they can pretty much come in. However, we have another cohort for DBS patients, and there we have a little bit more stricter inclusion criteria. We are making sure that they are okay in terms of Hoehn and Yahr one, two, three and MMSE 21- 30. I told you we are measuring a lot of stuff, and look at everything we measure. The reason is that while we obviously want to see safety, we want to understand in this patient population how the drug really works. By measuring not just safety, but different scales for movement, different scales for cognition, and a lot of biomarkers, it's going to tell us not just neurofilament light, but all inflammatory factors, all other biomarkers that have been associated with Parkinson's or Alzheimer's disease. We are measuring them both and how they change in Parkinson's disease. We also have some innovative biomarkers in there. We have a NeuroRPM watch, which is a watch that syncs with the iPhone, and it actually measures movement. Then we have alpha-synuclein skin biopsies. What we can see in skin is, A, are there alpha-synuclein aggregates? We can also see nerve cell fiber density. If a nerve is healthy, it has a lot of fibers in the skin. If a nerve is dying, the fibers are dying, and there are less fibers there. That is what we're doing in the open label. Just like in Alzheimer's, we're taking a step back to see how we got to the two studies we are doing. Our phase III Parkinson's study was two doses. Again, we only asked the PI to decide if a patients had or did not have Parkinson's. We took the endpoint the FDA told us to use, which was UPDRS2. Again, just like in Alzheimer's, the intent to treat population did not work. However, when we did look at the per-protocol population, we saw an improvement in UPDRS2, 3, 4, and total. In a per-protocol population, we actually saw that the drug works. We would like to understand this per-protocol population better with biomarkers, so that when we do a real Parkinson's study, we can actually select the people that do respond. What we saw, however, that is a very strong, not just signal, but actually statistical significant outcome, is that Parkinson's patients improved in cognition. This is not something we were looking for. We found it after the fact. In fact, on the very left, you see that the total population, the placebo patients get a little worse, and the two treated groups remain the same. They don't get worse. If we then take the patients that have an MMSE between 20 and 26, which means they're slightly mentally impaired, we see that both doses improve cognition. Then we went a step further, and we analyzed these patients on whether they had amyloid pathology or not. This means, do they have Alzheimer's and Parkinson's? What we saw is, on the very, very right, that the patients that had plaques, tangles, and Lewy bodies, these are our Alzheimer's and Parkinson's patients mixed, that these patients show a huge decrease in cognition and a large improvement with our drug. If we look at the patients that do not have amyloid pathology, we don't see any change. They don't change in six months. Then we looked at, interestingly enough, Alzheimer's biomarkers in Parkinson's patients. What we see is the p-tau217 in plasma that represents plaque decreases. They have less plaque. The BD tau that represents tangles decreases. They have less tangles. The total tau decreases. In Parkinson's patients with amyloid pathology, we can show that amyloid pathology decreases. We do not know yet if Parkinson's pathology decreases because skin sample for Parkinson's disease was just invented, and we are doing the study right now. Let me summarize why we are so confident that our drug works in cognition. In patients that are amyloid positive, tau positive, independent of Alzheimer's or Parkinson's, and have an MMSE over 20, our drug improves cognition. We saw that on the very left in a nine and 14-patient study. You see that placebo in each case improves by one ADAS-Cog point, and the purple bars improve by three to four ADAS-Cog points. That is true for very few patients. Next to that, you see the study I already showed you, where the pink bar showed the best improvement, again, 3.5 ADAS-Cog points, which is the patients we are doing now in our existing study. Then I am showing you the three Parkinson's groups that respond, the total, the mildly demented ones, and then the most and best response from the amyloid positive ones. I think most of you have seen this, but I am going to say it again because we are getting closer to reality, to the reality check. The green line is the natural disease progression for Alzheimer's disease. Alzheimer patients deteriorate by about 3.5 ADAS-Cog points per year. If you look at the red line, this is Aricept or Exelon. Patients improve by 1.5 points for six to nine months. This is six months improvement. If you look at the blue line, Leqembi and Kisunla, they do not improve. But what they do, they slow the progression by 1.5 points. This is, again, six months. This is our drug. We have shown in one month, three month, and six months data that our drug improves cognition by three to four ADAS-Cog points. We will prove this in March of next year. Then the question is it disease modifying or not? If we look at the data we have in inflammatory factors, in BD tau and p-tau217 biomarkers, if we look at NFL, I would tell you that, yes, our drug is disease modifying. But it is going to take us another 12 months to figure that one out. All of you want to know, so when will we have what data? In October, the first patients will, actually only three, they will be done with the 18-month study and become eligible to go into the open label. By December 26th of this year, we will complete enrollment for the Parkinson's open label study. Then also December of this year, it is the last person, last visit for the six months pivotal phase III study. After that, we will have to clean the data, analyze the data, and then present the data at ADPD, which is in the middle of March of next year. That will be the six month symptomatic data. We have a two-hour panel at ADPD, so we better have the data. By May 2027, we will start filing the NDA. We are actually starting to do some models now, and we will file as we go. But by May, we should be somewhat advanced in filing the NDA. March of 2028, similar to March of 2027, we will have the top-line data readout. Again, it fits nicely with ADPD for disease modification. In April, we will add the data to the existing NDA for disease modification. I told you about the Parkinson's disease dementia study, and that will wait until we have enough funding to do so. That is it. Thank you very much. Thank you, Dr. Maccecchini, for that comprehensive update on the company's progress. We will now move to the Q&A portion of the webcast. As a reminder, if you have a question, please use the Q&A feature in your webcast interface located at the bottom of your Zoom screen. Let's get started. The first question that we have here for you, Dr. Maria, is, does Annovis expect to release any interim clinical cognitive NeuroRPM or alpha-synuclein data from the Parkinson's open-label study before the Alzheimer's top-line readout? The first part is yes, the second part is no. Let me explain. It does not make sense to release data every two or three months because nothing changes. While we are measuring every six months, alpha-synuclein in skin and NeuroRPM is continuous, but really and honestly, we have to wait for the disease to progress somewhat before we can really say something. Yes, we will release data, but it will be either after most of the patients have been in the study for 6 months or after one year, depending on how the data looks. Okay. Very good. Thank you. Next question, if the six month Alzheimer's study meets its pre-specified efficacy requirements, what additional steps would remain before Annovis could submit an NDA? Say that again. What are the remaining steps? What additional steps would remain before Annovis can submit an NDA? Nothing. We can submit an NDA. That's why we're starting to work on it now. Basically, what we're trying to do is have most everything ready other than the efficacy, so that one to two or maybe three months after we have the data, we have put everything we have into the FDA so they can review it. All right, great. Perfect. Next question. After the NDA submission, how does management plan to fund commercial operations and scale up without relying on further equity offerings? That's a great question. Now I'm going to tell you that I'm a little chicken, okay? Ideally, we should start now. But if the six months data is good, we'll go full-blown into commercial. If the six-month data isn't good, I'm going to really, really have a hard time raising enough money to do the 12 months. That's why I'm a little chicken, because I'm starting something I may not be able to finance. All right. Thank you for that. One last question before we open the floor to open live questions. It is, what are the plans regarding buntanetap and the EU market for Parkinson's post FDA approval? How much time is needed to get EU approval? That's a great question because we actually have just been talking to several EU regulatory consultants. We have talked to the European Alzheimer's Association. We started to make contacts. We very much plan to file with the EMA, two things. One is the ongoing Alzheimer's study, and the other one is the not-yet-started Parkinson's disease dementia study, and we plan to do that later in fall, later this year. Okay, great. Well, thank you for answering those. Now we can open the floor for live questions. So if you have a question to ask, please raise your hand. I see one hand raised. They've been waiting patiently. I'm going to allow you to talk. You can unmute yourself, Bubalon. Hi, good afternoon. Can you hear me okay? Yes. Perfect. All right, great. Thank you so much for the presentation. A couple of questions from us. Firstly, your phase III criterion is a Phospho-Tau 217/t-tau ratio of greater than 4.2. Most recently, as you may know, Roche has just cleared an absolute p-tau217 assay, and they have their own cutoff and- Yes For positive and intermediate negative structure. Right. Based off of this, which assay and cutoff would you plan to use in the NDA's biomarker-defined population, assuming you go to the filing stage? That's a great question. You looked very carefully. You're right. We used the ratio in our previous study. We discussed it with the FDA. They said, don't use the ratio. In this study, we are actually using p-tau217, exactly what Roche and Eli Lilly are doing. Okay. That is very helpful. Then, maybe just for the discussion's sake, can you maybe tell us a little bit, is the six months analysis pre-specified with alpha control? Also, who has access to the first quarter 2027 database lock? Is the sponsor or Annovis firewall? Yeah. The FDA was very clear about that, and we discussed it quite in detail. There is a firewall, okay? We had to pretty much hire a totally independent team. It is not the CRO, it is not the PI, it is not the KOLs, it is not the company. It is a total independent team. We have one medical doctor, three statisticians, two scientific somethings, and two regulatory or three regulatory people. So they will have access to the blinded data. They will also file the NDA, okay? Because we do not have access to the actual data. We can just see the top-line data, which we will get, and then we can report that to the public. Okay. So just to be clear, the FDA has agreed that publishing six months top line does not compromise the 18 months primary? No. The way we are doing it does not. Okay, fantastic. Maybe one last question. Can you maybe briefly comment on the quarterly R&D run rate until or through the first quarter 2027 lock? Thank you. Yes. So we recruited too many patients. I'm happy we did because it will help our statistics, but we have too many patients, and we don't have enough money to make it to read out. We will have to raise money before Christmas. Okay. Thank you very much. Thank you so much for the great questions. We have some questions coming in in the Q&A. Remember, you're welcome to raise your hand if you'd like to launch your question live. A question that came in from the Q&A box is, are biomarker options other than the skin biopsy under consideration for the Parkinson's programs? Well, there are really only two. One is the skin and the other is the precipitation assay in CSF. The reason we chose the skin, at this point, it's hard to say, but there is a chance. There is a chance that in skin we can see progression. We know that in the precipitation assay, it's either yes or no. There is no progression. We can't see that. So we feel that we take the chance that maybe we can see progression with skin samples. In both cases, we'll see yes, no. Okay. Thank you for that. Another question from the Q&A box. Have you considered testing smell in Parkinson's? Smile? Smell. Good question. No, we haven't. Well, it just depends how many things do you want to do to your patients. Smell is not that specific. Smell also goes away in Alzheimer's, so no, we haven't. Okay. I saw a hand pop up there. I lost it, though. Okay. Someone had raised their hand there. Don't be shy. There we go. Paolo Matias, your mic is available to open up. Can you click and unmute your mic there, Paolo? Can you hear me? Yes, can you hear me? Yes. Okay. Basically, we're talking about the main situation be resolved by 2028. I would like to know if you have enough money to finish this project. If you don't have, what will be the solution for the situation that you have on? Well, Paolo, I have never- Yeah had enough money to finish anything I started. That's not unusual for me. We'll raise money. How you going to make money? How are you going to make, is your shareholders are able to invest more money on your company? Because I am a shareholder for your company. Yes. I've been buying. It has not been good. I'm really sorry about this. Our stock has been terrible to shareholders. Yeah. I'm really sorry about this. I'm asked why. Unfortunately, Alzheimer's is not a good thing to invest in. I'm not telling you not to invest, but let me explain. Out of 10 companies that existed 7- 10 years ago, all with brand-new ways of treating Alzheimer's disease, every single one of them, we didn't have the same way. We had different ways. They were all different from A-beta. I thought that was so fantastic. We could actually really understand the brain, because if you approach this from so many different parts, every part is going to tell you something. You know what happened to those companies? They either changed or don't exist. As far as I can tell, we are the only one surviving. Statistically speaking, we should be dead, right? Yeah. I believe that also, and I am very enthusiastic about your project. I live in Brazil. Yep. When I start reading about your company, I feel very excited. I start buying from about five years ago, anyway. Higher, lower. I think you are on the right path because everything is there, and I think they did not realize, the investors, how much future your company has. I hope they will understand before it is too late for them. Okay? I like to congratulate you for all the work you have been putting on this project. Thank you. Thank you so much. You know what? I cannot do much about the stock, but I can do a lot about the drug, and we are going to get it approved. That is the situation, and that is why I trust you so much, and I think you are going to do that. Okay? Thank you very much for your time. Thank you. Thank you, Paolo. All right. From Charles Overy, your mic is enabled. Go ahead. Are you able to click on your microphone, Charles, and open it up? Charles Overy. Oh, sorry, we're not able to hear you. There's a little red line on your microphone. Are you able to click there and open it up? Sorry about that. Okay. In the meantime, I saw a couple other hands. Let's see. I think we have another question in from the chat box in the meantime. Are there any discussions or potential partner conversations occurring? Well, not really. I mean, pharma knows about us, but pharma has decided they're waiting for 18 months data. In some ways, I understand why. If it's a symptomatic drug, it sells into a generic market. They're not interested in that. If it is a disease-modifying drug, it's a once-a-day pill, it has way less side effects or no side effects, then they will be interested in a disease-modifying drug. Okay. Thank you for that. I think Charles hasn't been able to open up his mic. Sorry about that, Charles. Another question came in from the chat. Enrollment in the AD study, is it limited by the p-tau217 test at 67%? Will this limit the 100 M market op? The two biggest screen fails were MMSE, patients came in too early or too late, and the p-tau217. MRI didn't exclude too many people. Comorbidities did exclude some people. We didn't take people with renal insufficiency, with liver problems, with, not undiagnosed, but uncontrolled diabetes, uncontrolled high blood pressure. The two biggest exclusions were MMSE and p-tau217. Okay, great. Nand Kishore, your mic is available to open up. We'd love to hear from you. Go ahead, and there you go. Hi, Maria. How much do you plan to raise before Christmas, and would this be the last raise that you would raise from the market, or how does that look like? Well, given our market cap, we cannot raise $70 million. Okay. So we raise about 15. That gets us into April, May. After March, we have to raise for the additional 12 months. Okay. Thank you. Thanks so much, Nand. There's a question coming in. You're welcome to raise your hand there, anyone who would like to shoot out their question. A question from the chat box is, or the Q&A box, sorry, will you be able to release the 30 mg dose in 2027 for AD modification until the 18-month study is accepted by big pharma? Yeah, we will release the six-month study. Yes, we will release that in March. Yes. Perfect. Okay. Anything else you want to mention, Maria, until some other questions come in? I think we've answered all. No, I'm really, really excited we have made it this far. 860 patients is an achievement, and we did it in record time. Now I'm excited that we have another five months to clean data like crazy. We'll be ready in January. Fantastic. Thank. I'm going to give you an update in March. Mm-hmm. One more question did come in. Okay. I'll launch that for you. Do you consider genetics during trials, for example, by measuring the effects of the drug in genetic subgroups? That's a good question. Given the mechanism of our drug, it doesn't act on the genes. It acts on the mRNA. It actually does nothing to the genes. Genetics shouldn't make any difference. Now, whether at some point we want to maybe, I don't know, look at something, but the question is, we don't know what to look at. Because if you have a drug that specifically targets a mutation, then you know what to look at. But we are not targeting anything in the genome. We are targeting mRNAs, and that is post-genomic. The DNA makes the RNA. I can't really say no, because if a really new study came along or some new technology that is very interesting, we may try it, but I don't think so. Right. Thank you. Next question that came through the Q&A. How does your current cash burn rate step down in back half of 2026, H2, and 2027 first quarter? Yeah, we had a real step-up in cash burn in first and second quarter because we were screening over 2,000 patients to get the 660 enrolled. So we screened a lot of patients. A screen costs anywhere between $10,000 and $15,000 per patient, depending on where they drop out. So yeah, the burn is going down, but it's not going down that much because every 6 months, on the patients we have, we still do volumetric MRI and p-tau217. We don't do it as a screening, but we do it as a continuous studying of their trajectory. Is the volumetric MRI going up, down, or sideways? Is their brain shrinking? Is their p-tau going up, down, or not? Do they have less plaque in their brain? So yes, we will spend less money going forward, but it's not going to be that much less. Perfect. Okay, next question. You intend to commercialize the drug post PD six months readout. How much revenue do you expect? No, we don't intend to commercialize post six months. The reason is that it's going to take the FDA, I don't know, a year to do an NDA. If we want to commercialize after disease modification. The way it works is if we have everything ready for the NDA, then wait for the 18 months readout, we don't have to file a new NDA. We just file an addition to the existing NDA, and that's only a three month review time. Everything will be ready, four to six months, then we add the 18 months, and that only takes another three months, not a year. That's why we are starting the NDA after the six months, even though the commercialization will be at 18 months. Fantastic. Okay. There are quite a few questions coming in the Q&A now. I think there's a nice comment. On behalf of all Parkinson's patients in New Zealand, thank you so much for your efforts. Thank you. How long will it take for the FDA approval after success of the full study? Well, if we are good, three months. If in fact the NDA, the one we are filing at six months is really good, then by March, it's going to take us a few months to put in the 18-month data, and then another three months. So it should be summer of 2028, if we don't make any mistakes, and if there are no hiccups, if nothing terrible happens. Great. Next question. What is our burn rate per month? I would say $7 million, $8 million, $9 million. It's a little, but the reason I say this is we came off these two very, very heavy quarters, and I don't have third quarter yet. Once I have third quarter, I'll know exactly what it is. Okay. What is your confidence level of the $19 million will last through April and May? What will last through April and May? The $19 million. Oh, it won't. Sorry. I need $15 million to make it last through April and May. Yeah, I thought I was clear. This money we have will last us into Q4, and we need to raise money before then, and then we're going to have April, May. Okay, great. Have you considered securing philanthropic funding or strategic partnerships through Alzheimer's patient advocacy associations to support clinical development? It's hard. Everybody asks me about philanthropy. I don't think that people understand that Alzheimer groups don't have enough money. This study costs $120 million. They give you half a million, they give you a million, they give you a max of 2, 3 million. It's nowhere. They can support me because they like the drug. They don't have $120 million. That is one of the fallacies. It's just reality. People don't understand how expensive these studies are, and that the Alzheimer's Association can't pay for it. That's the biggest Alzheimer group we have in the U.S. If they wanted to pay for it, they would have to give us two years of their philanthropy. That's not realistic. Got it. Thank you. Okay. Great questions coming in here. Would you expect buntanetap to be more or less effective in Parkinson's patients with severe dementia compared to mild dementia? No, I expect it to be very effective in mild dementia. Remember I was saying that when we looked at MMSE 14 to 20 in Alzheimer's, it didn't work very well, whereas when we looked at MMSE over 20 in Alzheimer's, it worked excellently well. In Parkinson's, we didn't have severely demented patients because we only recruited over 20. We saw, though, that MMSE 20 to 26, they responded very well. Unfortunately, I don't think it's going to work in severe dementia. Okay. Good. Next question. Finances and statistics aside, thank you from your patients who are already feeling better from all your hard work and investments. That was a nice comment, not a question. Thank you. Thank you. Very nice. Would Annovis Bio consider marketing the drug itself? Yes. It will simply be a very simple calculation. It is called return on investment. I am a scientist, but I, by default, had to learn finances, so it is return on investment. Okay. All right, we'll take one more question, I think. We're almost getting to the end of our time here together. Is there an update from the DSMB since January, February, and will the raise in December be partially bought by insiders? DSMB, yes. We have another DSMB at six months, so that will coincide with our six months data. We haven't had any serious adverse events, so we haven't called the DSMB, but we'll definitely have one at the end of the year, which coincides with data. In terms of the second part, which was? Brooke, what was the second part of the question? Good question. Let me grab that. Will the raise in December be partially bought by insiders? Yes. Our chairman will invest, I will invest, maybe somebody else will invest. The two of us, we have already said we will invest. Yeah. Perfect. I see hands coming up, so we'll definitely take those. First Brendan, and then Robert. Brendan, you are able to open your mic there. Hello. Just had a quick question on what role does neurofilament light play into the progression of Parkinson's, from your understanding, please? Well, neurofilament light shows the health of a nerve cell, so it's a distress factor for nerve cells. If nerve cells are unhappy, they scream and neurofilament light comes out. If they're happy, they make less of it. And that we have seen in Alzheimer's and in Parkinson's, and obviously it is in ALS. So it's a marker that tells you how happy nerve cells are. Okay. Thank you. Thank you, Brendan. Robert Northworthy, you are able to open up your mic there. Okay. Can you hear me okay? Yes. Yeah, I just had a. I do not really know how these things work. Would it be possible for Parkinson's patients, if you were to have your drug accepted or your new drug application accepted, could Parkinson's patients take the drug off-label? Well, absolutely. I do want to develop it for Alzheimer's and Parkinson's. But realistically, once it is on the market, you can get your doctor to prescribe it for anything. I really think we should get it approved for Parkinson's, and I will do my best to do that. But if ALS, we have organoid data that it works in ALS, that is not published yet. We have a ways to go. But if there is a paper out there that says the drug works in an ALS organoid and it is not approved for ALS, the doctor will prescribe it. Well, that is outstanding. Okay, thank you. Thank you, Robert. And thank you everyone for your great questions, very insightful, and for participating in today's webcast. We truly appreciate your engagement and your interest in Annovis Bio. That will finalize Thank you very much. Yeah. Just as a reminder, a replay of today's webcast will be available on our website. And thank you again for joining us. Thank you, Dr. Maria Maccecchini, as well. Have a great evening, everyone.