Cognition Therapeutics, Inc. presented results of a meta-analysis from the first cohort (SHINE-A) of 24 participants in the Phase 2 SHINE (COG0201; NCT03507790) and the complete dataset from the Phase 1b SPARC (COG0105; NCT03493282) studies in adults with mild-to-moderate Alzheimer's disease who were treated with either CT1812 or placebo. Treatment with CT1812 was associated with statistically significant and directionally positive effects on key proteins and corresponding Alzheimer's disease pathways. These included: Synapse health; Neuroinflammation and amyloid-b (Ab) biology.

These robust biomarker findings point towards a prominent effect of CT1812 in altering underlying disease processes active in Alzheimer's disease progression. Of particular note, CT1812 had a significant impact on CSF levels of clusterin (CLU), which has been identified as a genetic risk factor for Alzheimer's disease and is a mediator of amyloid toxicity. In addition, CT1812 treatment resulted in a significant shift in levels of prion protein (PRPN), a major constituent of the Aß oligomer receptor complex and the receptor component to which Aß oligomers bind.

The biomarker findings summarized in the poster further strengthen understanding of CT1812's effect on Aß oligomer-driven neurotoxicity.