Cognition Therapeutics Initiates NIA-Funded SNAP study of Elayta™ to Measure Toxic Oligomer Displacement and Clearance in Alzheimer’s Disease

PITTSBURGH, June 5, 2018 — Cognition Therapeutics, Inc., a clinical stage neuroscience company focused on the development of innovative therapeutics for the treatment of Alzheimer’s disease and other neurocognitive disorders, today announced that the first patient has been dosed in the SNAP (AβO Displacement from Synapses on Neurons in Alzheimer’s Patients) Study of Elayta™ (CT1812), Cognition’s lead candidate for the treatment of mild-to-moderate Alzheimer’s disease (AD). The SNAP Study is enrolling patients at the University of Pennsylvania School of Medicine under the direction of Yvette I. Sheline, M.D., the McLure Professor of Psychiatry and Behavioral Research.

In the SNAP study, up to 18 mild-to-moderate AD patients who are positive for beta amyloid (Aβ) will be randomized to receive a single dose of either Elayta or placebo. Cerebrospinal fluid (CSF) of study participants will be sampled at baseline and hourly for 24 hours and the concentration of Aβ oligomers (AβOs) in the CSF will be measured using novel highly sensitive methods of AβO measurement pioneered by Cognition and John R. Cirrito, Ph.D., associate professor of neurology at the Washington University School of Medicine.

“This ground-breaking study promises to provide new insights into AD and Elayta’s mechanism of action and confirm Elayta’s ability to displace toxic AβOs from their synaptic binding sites and clear them into the CSF,” said Dr. Sheline.

Preclinical studies in mice demonstrated that AβOs were displaced from their neuronal binding site by a single dose of Elayta and cleared out of the brain into the CSF. Data from these studies, conducted by Dr. Cirrito and his colleague Carla M. Yuede, Ph.D., were presented at a late breaking session at the Clinical Trials on Alzheimer’s Disease meeting in November 2017. The SNAP study is designed to evaluate whether the same displacement and clearance results can be observed in Alzheimer’s patients.

“While studies have suggested that clearing toxic AβOs out of the brain would have a synaptoprotective effect in AD patients, oligomers are present at such low concentrations in the CSF that we had to develop fundamentally new methods of detection in order to measure them,” said Dr. Cirrito. “This study is the first in the world to use these novel methods, and therefore we expect it will shed light on baseline concentrations of AβOs in AD patients as well as how the concentrations change after dosing with Elayta.”

Alzheimer’s disease patients experience a degeneration of dendritic spines and synapses, caused in part by the binding of toxic AβOs. A previous clinical trial in AD patients dosed with Elayta once daily for 28 days, also presented at a late breaking session at the November 2017 CTAD meeting, demonstrated significant lowering of synaptic damage markers in the CSF.

“Elayta is unique among Alzheimer’s candidate therapeutics in that it does not directly interact with Aβ protein species or affect their production, but rather produces its synaptoprotective effect on brain cells by altering the binding of AβOs to their synaptic receptor proteins and clearing them out of the brain where the disease is devastating synapses,” explained Cognition’s co-founder and Chief Science Officer Susan Catalano, Ph.D. “We look forward to working with Drs. Sheline and Cirrito to further our understanding of Elayta’s mechanism of action and pharmacodynamics, which will be of great importance as we advance this novel candidate through clinical development.”

The SNAP Study, formally “A Pilot Study to Evaluate the Effect of CT1812 Treatment on A-beta Oligomer Displacement into CSF in Subjects with Mild to Moderate Alzheimer’s Disease,” is funded by a $2.5 million NIH grant from the National Institute on Aging (NIA) (award number RF1AG057780), which is one of a number of NIA grants supporting the clinical development of Elayta. More information may be found at under trial identifier NCT03522129.

About Elayta (CT1812)
Cognition’s lead product candidate, Elayta (CT1812), is a highly brain penetrant small molecule with a unique disease-modifying synaptoprotective mechanism of action. This orally dosed drug candidate protects synapses by selectively displacing toxic AβOs from their synaptic receptors, thus stopping downstream damage. Elayta has been shown in preclinical models of Alzheimer’s disease to restore synapse numbers and improve memory function. Consistent with these findings, Cognition’s Phase 1b/2a clinical trial demonstrated that Elayta significantly reduces concentrations of synapse damage proteins in the cerebrospinal fluid of Alzheimer’s patients. Elayta is currently in Phase 2 clinical testing for mild-to-moderate Alzheimer’s disease and has been granted Fast Track designation by the U.S. FDA.

About Cognition Therapeutics, Inc.
Cognition Therapeutics is a privately held biopharmaceutical company developing a pipeline of disease modifying small molecule drug candidates to treat neurocognitive disorders. Cognition’s lead candidate, Elayta, is a proprietary first-in-class, orally available small molecule in development for the treatment of mild-to-moderate Alzheimer’s disease. Elayta and Cognition’s other pipeline candidates were identified using the company’s disease-relevant screening and novel chemistry platforms. Additional information about Cognition and its product candidates may be found online at

Forward-Looking Statements
This press release contains “forward-looking statements” concerning the development and commercialization of Cognition’s products, the potential benefits and attributes of such products, and Cognition’s expectations regarding its prospects. Forward-looking statements are subject to risks, assumptions and uncertainties that could cause actual future events or results to differ materially from such statements. These statements are made as of the date of this press release. Actual results may vary. Cognition undertakes no obligation to update any forward-looking statements for any reason.

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