We are going to get kicked off here. You all good with my mute? Okay, awesome. Yeah. I don't need much warm up. Okay. For my next introduction. I thought we were not going to do that. I had to do it. Neil Warma in the house. Let's hear it. With ProMIS Neurosciences. Neil Warma, CEO, biotech, developing therapeutic antibodies for neurodegenerative diseases like Alzheimer's and ALS. Big round of applause for Neil. Take it away, my friend. Thanks so much. Thanks for the warm introduction. Careful how you pronounce that. But yeah, thanks everybody for joining for the next few minutes. Neil Warma, CEO of ProMIS Neurosciences, and anybody who was sitting in the last presentation, this will be a little bit of a shift from data centers. This is all about potentially curing neurodegenerative disease, Alzheimer's, ALS, Parkinson's disease is our focus. I will walk you through. I will not get too heavy into the science, but it is a science-based company. I will walk you through some of the science. Just to remind everybody, we are a publicly traded company, so I will refer you to the SEC file documents on the SEC website as well. With respect to ProMIS Neurosciences, and a way to maybe remember us a little bit better after today is the name ProMIS. In addition to the promise of novel, safe, and effective drugs to patients, our technology is based on protein misfolding. The effects of misfolded proteins on a number of different diseases. ProMIS, protein misfolding. We are a publicly traded company, as I mentioned, the ticker's PMN, trading on the Nasdaq Capital Market exchange. We have been public for a number of years. I have been CEO for about two and a half years. I have been on the board for longer than that, and I have a neuroscience background. Joined also by our Chief Medical Officer in the audience, Dr. Larry Altstiel, who is a practicing neurologist and with vast amounts of development expertise as well. We have a product in the clinic. We are a clinical stage company, and I will speak a little bit about our, fairly a lot about our clinical stage asset in Alzheimer's disease. The market in Alzheimer's disease is significant. Huge unmet medical need. From a financial perspective, we are financed quite well. We did a relatively large financing back in February of this year. A few months ago, we raised up to $175 million from some of the top long-term institutional investors in the biotech space. We were thrilled with that. Outstanding team managing the company. Again, we pride ourselves on our differentiation of our technology. I will not speak too much about the technology, but I will come back to that in a minute. I will spend a few minutes, towards the middle part of the presentation, talking about some of our clinical data. Obviously, the value in biotech pharma companies is generated by solid clinical data. We had an interim read back on July 28. We are well on our way through an Alzheimer's trial right now. We had an interim analysis we presented at the end of July, which is actually quite encouraging. It was blinded. It was a six-month analysis. I will point to a few data slides in a minute. Again, what it showed us is the product appears to be very safe with a much better safety profile than the drugs on the market. We showed what we believe to be some strong target engagement as well. A really nice interim signal came a month or two ago en route to the final data package, which comes in about six months from now. We have guided to top line final results in our Alzheimer's study in Q1 of 2027. A number of months from now, we should be able to unveil the top line unblinded data, and ideally speak about a really transformational product for the treatment of Alzheimer's disease. Our technology, just kind of briefly, again, around protein misfolding, and as you guys probably maybe remember from your biology classes a few years ago, that proteins are manufactured by the cell, and they typically come out of the cellular machinery in a very elegant three-dimensionally folded. They fold upon themselves, and you have got this elegant shape of the protein, which then goes off to perform its task. Continuously, proteins come out the cellular machinery, and they are misfolded or folded improperly. These can be very harmful. Your immune system typically takes care of these, grabs hold of the misfolded proteins and clears them from circulation. Because if they are allowed to accumulate and build up, the misfolded proteins, they can cause some serious diseases as the ones listed here. Our technology, because sometimes when people get a little bit older, immune compromised, they can't clear these misfolded proteins, and then they are allowed to aggregate and build up and cause all sorts of trouble. Our technology, we have the ability to predict how proteins are going to misfold, and it's a really elegant process. It's kind of AI back in the days when AI wasn't even known or really cool to talk about. But we have a chief physics officer, and together we have a computational modeling that allows us to predict how proteins are going to misfold, and we design our antibody, our therapies, our monoclonal antibodies, and the antibodies specifically target these misfolded epitopes. And these misfolded epitopes, our binding domains exist only on the misfolded form of the protein we're targeting. Makes us truly unique in the design of our antibodies, which is critical to our platform here. Different proteins are associated with different diseases. For Alzheimer's disease, we're looking at a second-generation antibody targeting beta-amyloid. Aβ protein is a known target for Alzheimer's disease, so that's our target, I'll come back to that in a minute, for the Alzheimer's program. Beyond Alzheimer's, we're looking at misfolded form of TDP-43, which is known to cause ALS. That's our next potential clinical candidate. We're looking at misfolded forms of alpha-synuclein, which is responsible for a number of different diseases, including Parkinson's disease and Lewy body dementia. Different misfolded proteins are implicated in different diseases. We have a relatively healthy pipeline of a number of neurodegenerative diseases. This slide is interesting because when we talk about Alzheimer's, we come back to the Alzheimer's indication, and we're focused on, as I mentioned, amyloid beta protein. That's the target that Eli Lilly's gone after with donanemab, that's the target that Eisai Biogen have gone after with lecanemab. The challenge is there's different species or subspecies of amyloid beta protein, and some are beneficial. You've got the monomers. The monomeric species of amyloid beta is beneficial. It has a biological function. You don't want to touch this if you can help it. The next is a plaque. We're all aware of the plaque depositions in the brain caused by beta-amyloid buildup in the brain. It was thought years ago that that was the relevant target for Alzheimer's drugs, that if we can clear plaque, everything will be fine. We now know that, and there are drugs that completely remove plaque, and the patients continue to decline. It's like, hmm, so it's not plaque, there's something else there. Not only that, and this is important, the drugs that target and bind plaque and remove them, are now associated with a very serious side effect, so swelling and bleeding on the brain. Not only is there not much cognitive benefit to the Alzheimer's patient by clearing plaque, you've also got this horrible side effect, bleeding and swelling on the brain. Now the field has come back to, over the past number of years, these toxic oligomers, which are much lower concentration than the monomers and the plaque. Now we know that it's these upstream low molecular weight oligomers that if left alone, they go downstream and form plaque, but their destructive properties come early on, and they're highly destructive to neurons, especially the synapses. That's the species that everybody's trying to target now. But the challenge has become, well, it's all beta-amyloid protein, so how can you pick and choose which ones you're going to hit? Because it's the same epitope that's consistent across everything. But that's when it comes back to the beauty of our platform. We actually, again, predict and identify a binding domain, a binding epitope that only exists on the toxic oligomers. So our antibody only hits this, it avoids plaque, and it certainly avoids the monomers. So we're truly differentiated in the ability to go after these highly toxic species of beta-amyloid. And that makes us unique. Others have tried and claimed that. Lecanemab, the drug on the market by Eisai Biogen, was designed to go after the oligomers. But again, because they don't have our technology and the ability to be personalized or precise, they hit them all. So lecanemab binds everything. It also binds the oligomers, which gives it its a little bit of efficacy, but it's associated with significant ARIA, the swelling and bleeding on the brain. So that's a little bit. And we, again, I won't go into this, we spent a lot of time looking at are we differentiated, do we bind plaque or can we actually state and claim that we don't bind plaque? We believe we will not show a significant swelling, bleeding ARIA, as it's known, side effect issue. So we did head-to-head with all the other antibodies saying which ones bind plaque. And the green stains show that these are brain sections from Alzheimer's patients. The green shows there's plaque in the stains. The purple shows which antibodies bind the plaque. And all these guys do. So these are the ones on the market. Here's Acumen's product. And our product, PMN310, was the only one that did not bind plaque. And that's important because we went into the clinic saying, "We don't believe we're going to have this serious side effect issue known as ARIA." And that's highly differentiated because ARIA is a significant issue. So we marched forward. A little bit of background on the two products in the market. You've got lecanemab, donanemab from Lilly, as I mentioned earlier. Modest efficacy. Again, part of the challenge is administering your drug. If you're binding all forms of beta-amyloid, 90% of it gets soaked up by the monomers and the plaque. You remember the pyramid, there's much more plaque and monomers than there are the target you're going after. So they show a little bit of efficacy, which is demonstrated here, but they have serious levels of swelling and bleeding on the brain, ARIA. They've got a black box warning from FDA. So the risk-benefit of the drugs on the market is pretty poor, yet they're still projecting $3 billion, $4 billion in peak sales. But that's based more on the unmet need than the value those products are bringing to the market. So going into the clinic with all that, we did a phase I-A trial in healthy volunteers, product safe and well-tolerated. We designed probably one of the more comprehensive clinical trials for a first inpatient study, a phase I-B study. With the help of Dr. Altstiel and the clinical team, we wanted to design a study that was robust enough to give us a definitive answer whether this drug actually worked in Alzheimer's disease. Others before us had done more of a quick and dirty three-month, 30-patient study. It was important for us to say, "Let's run a study that's going to give us a definitive answer." That meant enough patients over enough time period to show a clinical signal. We said, let's have at least 100 patients, and let's go 12 months of treatment. Monthly doses for 12 months, and that will give us the chance to show whether at the end of 12 months, we have a clinical signal, which is critical. Throughout the process, we're also going to look at biomarkers, which are very well understood in Alzheimer's disease and important to demonstrate target engagement. Then obviously, the safety piece is critical for us because we're going into this saying, we believe we can significantly lower that swelling, bleeding ARIA side effect issue, which is plaguing the drugs in the market. It's a very well-designed study. Enrollments completed as of last year, 144 patients in the study, running out for 12 months. We got Fast Track designation by the FDA last year. We applied for it. They recognized it. Huge unmet medical need, and this drug has the potential to do something quite impressive. So Fast Track from the FDA. We're running this study. The one thing we built in is the interim data analysis. We said a little bit because we're a public company and 12 months is a long time to wait for data. We said, let's build in an interim analysis. We'll do a blinded analysis. Once everybody's been treated for six months instead of 12 months, we'll look on a blinded basis to say, how's the data looking? Are we on the right track? We did that analysis July 28th, we presented those data. I'll touch on those just for the remaining few minutes. Again, it's important to remember these are blinded data. It's aggregated placebo. Again, I should have mentioned this is a placebo-controlled, double-blind, randomized study. It's randomized 3- 1. So, three patients on active, one on placebo. Every four patients, three on active, one on placebo. Just as a little bit of background about the study, as I said, 144 patients were enrolled. The safety analysis included 136 of those patients. Very few dropouts in the study. Again, we have three ascending doses. So low, medium, high dose, if you will. Just as a little bit of background, the average age was about 73 years. More females to males, a little bit, which is pretty typical in the Alzheimer's population. Race was pretty mixed as well. Important, and I won't get into this, but the APOE4 carriers, and these are individuals carrying at least one or two of the APOE4 alleles that are more affected by Alzheimer's and certainly have a higher risk for ARIA, the side effects. It's an important patient population to evaluate. So a fairly standard patient population. We're going after early Alzheimer's patients. These are patients with mild cognitive impairment due to Alzheimer's disease. That is our target. A fairly well-designed trial. From a safety perspective, and this was critical, a lot of people were looking at safety saying, "Okay, we have this whole ARIA, we have this black box with the two drugs in the market. How do you guys compare with that?" It is blinded, but it could be a pretty clear signal. I think for us it was a pretty outstanding signal. When we look at this case of ARIA, there are two types of ARIA, as I say, swelling and bleeding. So ARIA-E, and the bleeding hemorrhage, ARIA-H. Two types of ARIA. ARIA-E tends to be much more severe. When we looked at six months, it is also interesting to note that in the previous studies with the two drugs on the market, 90% of all this bleeding, swelling ARIA came in the first six months. That is an even more important signal for us, at six months is more meaningful because you typically see drug affect ARIA in the first six months of dosing. What we saw at six months was zero cases of ARIA-E. We saw no treatment-related serious adverse events. We saw no treatment-related dropouts. The overall ARIA, which is this lesser but still important ARIA-H, tracked with placebo background rates because every Alzheimer's patients will have this spontaneous hemorrhage ARIA as they continue with Alzheimer's. There is this background rate, and I will show you a chart in a minute that we tracked with. Very impressive on the ARIA signal or lack thereof. Overall safety beyond that, very safe and well tolerated. We were thrilled with the safety perspective. If you look briefly on the ARIA charts, these are the two drugs on the market. This is what they showed in their clinical trials over the past number of years before they got to market. As I said, ARIA tends to occur in the first six months, and you can see with the Eli Lilly product, almost 24% ARIA cases in six months. Lecanemab was at 12%. We were at zero. I think there are a lot of people that thought, and this, again, blinded placebo and active, but since there are no cases of ARIA, one assumes there are no cases in the active patient population. When you look at the overall H plus E, you can see the numbers from the other two drugs. That was an 18-month trial. But when you look at six months, significantly higher than where we were, and we were tracking with this background placebo rate. Really a terrific result from the ARIA safety signal coming out of that interim analysis. The APOE4, the high-risk population, just to emphasize that again, you can see that the ARIA rates, ARIA-E with lecanemab, 30%, we are at zero. From a safety perspective, we are tracking really well. On the other side of the equation, because people can say, "Well, it is very safe. That is awesome. You guys have a much safer profile than the others on the market." But is it actually doing anything? Because you can be very safe and non-effective. Are you doing anything on the other side? We actually looked at that to say, well, let's look at the biomarkers because we're not going to look at the clinical signal in six months. We'll wait for 12 months to look at any clinical signal. Let's look at a couple of these key biomarkers, and if we can demonstrate something interesting there, the potential for the target engagement, that our drug is hitting its target and there's a drug effect, that would be pretty interesting. We looked at two biomarkers that are very relevant and two biomarkers that, in essence, should move early. P-tau217, not to get into the details, is a measure of disease progression. Very well understood biomarker. Everybody knows p-tau217. It's used to identify Alzheimer's patients. It's predictable for clinical outcomes. There's a lot of relevance in p-tau217. We know that over time, patients will increase their levels of this biomarker. P-tau217 will go up in time without any treatment. We know the slope of the line looks like that. What we saw, which we thought was pretty encouraging, our slope started to come down. We took an upward slope, and we reversed it. Again, this is combined placebo, 3- 1 placebo and active patients. We were able to kind of pull this curve down with a 15% reduction in p-tau217 in six months, which is pretty interesting, to say the least. Also, we looked at, well, how many patients out of the 136 we evaluated, how many actually declined in p-tau217 levels versus increased? Declined, you could say there's an improvement if they're declining and a worsening if they're increasing. Interestingly, it was about 68% declined to 31% increased. That's roughly tracking our 3-1 randomization. Really neat signal. Then we also look, there's another MTBR, microtubule binding region tau 243. Another biomarker, a little bit more downstream. It's kind of a nice bookend for 217, 243. We know that the trend will go up over time if untreated, and what we saw, very similar with MTBR-tau243, downward trend and roughly a 3- 1 tracking with our randomization code. Really interesting signal coming out of the interim analysis. Terrific safety. Potential really here for target engagement. It looks like something's going on on the other side. Again, blinded six months, you want to be careful how you position it. About as good as we were going into the interim, we were managing our expectations and we came out at the other end quite pleased. Just the last couple of slides here is that, from the interim analysis, I think it supports our differentiated mechanism. We think we are avoiding plaque, therefore should have lower ARIA, which we demonstrated. We had that clean safety profile. We had our target engagement that we believe shows the efficacy signal potential coming out of the interim. The APOE4, the high risk population, which actually can't get the drugs on the market. They're not even approved in Europe for these patients. They're so high risk. That patient population seems to be nicely addressed by PMN310. I won't get into this, but there's a whole push now by the drug companies to look at treating Alzheimer's patients even earlier in diagnosis, so before they're symptomatic. Again, which is a great thing to do. If you can catch patients even earlier, just as they're developing the underlying pathology of Alzheimer's disease and keep them there, that would be wonderful. But again, if you've got 30% chance of bleeding and swelling in your brain, you're not doing that. For us, coming with a clean product and sliding in there could be interesting. Last couple of slides here. Again, we're moving forward. As I said, we've got the top line results coming Q1 of next year, where we unblind all the data, and we also look at the clinical signal. That will be pretty interesting. We're also working on a subcutaneous formulation right now. We dose IV. Important to us will be to get to the market with a sub-Q formulation, so that process is going forward. We're getting ready for our next study. Again, one of the advantages of designing such a robust phase I-B study is that we believe we can then step right into a registration phase III study after this reads out, hopefully very well. We'll sit down with the FDA next year. Subject to their feedback, we can go straight to a registration study, so we've cut our time to market significantly if this all works out as we expect. We've got two other candidates, the ALS candidate I mentioned at the beginning, the Parkinson's disease candidate. Those are both moving forward in preclinical development as well. As my time's running out, just to kind of reposition the company. Truly differentiated platform allows us to create and design these highly selective antibodies. We've got one that's kind of demonstrating that differentiation now vis-à-vis the products on the market. We've got a great clinical signal. We've got some very near-term catalysts. We're financially quite strong. I think the disconnect between where we're trading today versus the potential of where this could get to in Q1, Q2 next year with the results is quite significant. We're confident in the ability of the team. We're pleased with the interim analysis and how that looked, and we're certainly excited about the potential in the next few months to unbind the data and ideally have a really, truly transformative product for the treatment of Alzheimer's disease, which we all need. Big round of applause for Neil Warma.