OUR APPROACH: The Cenna Solution

Cenna’s proprietary technology addresses the underlying cause of the disease, the inappropriate deposition of the toxic species, Aß, in the brains of patients with AD. The Company has developed a novel druggable target and has discovered several lead peptide compounds that are active in vivo. Our lead candidate P8 inhibits the production of Aß in vitro and in a transgenic mouse model of AD by over 50%, is stable and can be delivered to the brain.

Citation: Dewji NN, Singer SJ, Masliah E, Rockenstein E, Kim M, Harber M, et al. (2015) Peptides of Presenilin-1 Bind the Amyloid Precursor Protein Ectodomain and Offer a Novel and Specific Therapeutic Approach to Reduce ß-Amyloid in Alzheimer’s Disease. PLoS ONE 10(4): e0122451. doi:10.1371/journal.pone.0122451

Cenna’s novel technology inhibits the production of Aß by >50% in vitro and in a transgenic mouse model of Alzheimer’s disease Cenna’s approach is different, specific and interferes with only the reaction that produces Aß, as opposed to approaches that target the enzymes responsible for its cleavage from APP, ß- and γ-secretase, which can affect multiple reactions in cells.

Cenna’s approach to reducing Aß is completely different and our novel technology has demonstrated evidence of success in transgenic mice.

Earlier therapeutic attempts by others at lowering total Aß production were unsatisfactory as they directly targeted the catalytic activities of ß- or γ-secretase, enzymes known to hydrolyze other substrates as well as APP, many with critical cellular functions. We have a novel technology that does not target the secretases, which has yielded several potential peptide drug candidates, with the ability to inhibit the production of Aß in vitro and in a transgenic mouse model of AD.

Inhibition of Aß in Transgenic Mouse Brain

Cenna’s drug candidates are small peptides that bind APP and block it’s processing to Aß without affecting ß- or γ−secretase activities