So we are presenting a poster on developing a vaccine for Alzheimer’s disease. And this is a very exciting new area of research because now that we know that antibodies can have an effect in the CNS, so there are monoclonal antibodies that are currently approved for treatment of Alzheimer’s disease, lecanemab and donanemab, and we have our own PMN310, which is in a Phase Ib clinical trial to target A-beta oligomers...
So we are presenting a poster on developing a vaccine for Alzheimer’s disease. And this is a very exciting new area of research because now that we know that antibodies can have an effect in the CNS, so there are monoclonal antibodies that are currently approved for treatment of Alzheimer’s disease, lecanemab and donanemab, and we have our own PMN310, which is in a Phase Ib clinical trial to target A-beta oligomers. So knowing that antibodies can have an effect, that you can give monoclonal antibodies, that is passive immunization, now this opens the door to a new approach, which would be the next big step, which would be active immunization. So vaccination against A-beta oligomers so that the patients can make their own antibodies. And so we used our platform to model the folding, the misfolding of toxic oligomers to find regions that become exposed only on toxic oligomers of amyloid beta so that we can then put that in a vaccine. And this would be unique to A-beta oligomers, and the antibody response would then be focused on the A-beta oligomers. And that is what we are presenting on. We found four different conformational epitopes that are only on oligomers, not on monomers, and not on plaque. And we did vaccination studies in mice to see how they would respond to these epitopes. And as we intended, the antibody response was selective for toxic oligomers, did not bind monomers, did not bind plaque, which we did not want to bind. And then the next question was, of these four epitopes, which combination would you put in a vaccine to be the most effective? So there’s 15 possibilities of either one, two, three, or all four. And so what we did is take immune serum from these mice and these different combinations and see which one gave us the highest level of binding to a toxic oligomer enriched fraction from Alzheimer’s brain, so the driver of disease. And we found that the best combination was actually a single epitope, which turned out to be the target of our monoclonal antibody, PMN310, that is in clinical trials. So with this single epitope, we got maximal binding of toxic oligomers. And if PMN310 pans out in the clinic, this would definitely be supportive then for a vaccine approach with the epitope.
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