ProMIS Neurosciences Inc. Common Shares (ON) 12th Annual Cantor Fitzgerald Global Healthcare Conference
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Welcome to the Cantor Healthcare Conference. I'm Pete Stavropoulos, a biotech analyst with Cantor. With us, we have ProMIS Neurosciences. With that, I'd like to welcome ProMIS's CEO, Neil Warma, and CMO, Larry Altstiel.
Altsteel. Altstiel, sorry. I always get that one wrong.
Thank you for joining us and for your time. Let's start off with introduction of yourselves, followed by an overview of the company, including lead candidate, its status on near-term catalyst, financing, and runway.
Sure, happy to. Thanks Pete for the invitation. Thanks also to the Cantor group for inviting us to the conference. Appreciate it. My name Neil Warma, President and CEO of ProMIS Neurosciences. I've been on the board for a number of years. Been CEO for about two and a half years now. Happy to be leading the charge at ProMIS. Larry, I'll let you introduce.
I'm Larry Altstiel. I'm the Chief Medical Officer for ProMIS, and I've been with the company about three and a half years. I'm a neurologist, neuroscientist by trade.
So as far as the update overview of the company, where we stand now, actually quite interesting time for the company. We're excited to be here. A couple of elements to touch on. From a financing perspective, which is always important for emerging companies, we are well-financed. We did a relatively large financing a number of months ago, so we're financed through to the end of next year, 2027. So financially, fairly strong. Superb syndicate of investors who came in in that round a few months ago as well. Importantly, we're coming up on some very important milestones for us. Our clinical candidate, PMN310, is currently in the clinic in a relatively comprehensive, relatively large Phase 1b study for the treatment of Alzheimer's patients. We've recently had an interim data result, about a month and a half ago, a couple of months ago, which was quite positive.
We were pleased with that blinded interim analysis. But more importantly, we have a top line, kind of final top-line results coming in Q1. So in a matter of six months, give or take, we will unblind the data from the Alzheimer's study and look at top-line results in what could be a transformational treatment for Alzheimer's patients. We have a very unique differentiated monoclonal antibody which selectively targets the oligomer species of amyloid beta protein. So well-financed. Some very near-term milestones coming up that we're very excited about.
All right. When most hear about amyloid beta antibody therapies for Alzheimer's, they think about plaque reducers, like the approved drugs lecanemab and donanemab. However, the therapeutic hypothesis for our 310 is differentiated from the approved amyloid beta antibodies. Can you just give us a synopsis of the different A-beta species? How that it binds to, sort of how you design your antibody and a bit more about the MOA?
Well, yeah. I'll start- No, go ahead.
You can jump in. That's kind of an important point because we certainly believe in differentiation of the asset for any company, and that's where we stand. Really from the very beginning of ProMIS, our idea to design antibodies are selected for specific species of a protein based on the misfolding of that protein. Our whole premise is on being able to identify and predict how proteins are going to misfold. In fact, our name ProMIS- ProMIS is protein misfolding.
Yeah. But it's really the ability to design antibodies that selectively target a misfolded form of protein.
For us, that has been from day one the oligomer species of amyloid beta protein. There's multiple species of amyloid beta protein. There's the monomeric species, there's the oligomers, there's the plaque species. Important for us, years ago, we decided as the industry and the field was moving towards the oligomer species of amyloid beta being the most toxic and the one that really drives progression cognitive decline. We've seen over the years, there's been this shift away from plaque. Over the past few decades, clearing plaque, removing plaque was thought to be the be all to end all. That was where the cognitive decline emanated from. But now we know, and we have drugs that completely eliminate plaque and patients continue to decline.
Now the field has come back to, well, if it is not plaque, and also with plaque, as we know, removing plaque is not really sufficient to prevent or affect cognitive decline. We also know that drugs that clear plaque are also associated with this very serious side effect known as ARIA, so swelling and bleeding on the brain. Again, not much clinical benefit, but some safety issues with clearing plaque. The field has shifted more towards this upstream, these toxic oligomers, low molecular weight toxic oligomers, which are highly destructive to neurons, and that we now understand is driving cognitive decline in Alzheimer's patients. For us, the ability to design an antibody that can avoid certain amyloid beta protein, the monomers and the plaque, and selectively target only these toxic oligomers sets us apart from everybody else.
We firmly believe that we are the only company out there that has an antibody that can avoid the plaque species, the monomer species, and really go after these toxic oligomers. That seems to be a key point of differentiation to have a much improved safety profile and a solid efficacy profile as well.
Awesome. Larry, can you just expand a little bit on the oligomer hypothesis, what evidence actually points you towards oligomers being the disease-driving species?
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