ProMIS Neurosciences Inc. Common Shares (ON) Moody Capital Disruptive Growth & Life Science Conference

I thought we were not going to do that.

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 2 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 6-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 2 ago en route to the final data package, which comes in about 6 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.