Pittsburgh, March 6, 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 Dr. Susan Catalano, Cognition’s co-founder and chief science officer, will make an oral presentation at the annual meeting of the American Society of Experimental Neurotherapeutics (ASENT) on March 8, 2018. Dr. Catalano will present results from the Elayta™ Phase 1b/2a clinical study in mild-to-moderate Alzheimer’s disease patients demonstrating Elayta’s (CT1812) unique synaptoprotective mechanism of action.
|ASENT Session:||Pipeline Presentations: Part I|
|Title:||CT1812 exhibits evidence of synaptic preservation in Alzheimer’s disease patients|
|Authors:||Catalano SM, Schneider LS, DeKosky S, Morgan R, Rehak C, Silky C, Mozzoni K, Izzo NJ, Grundman M, Schirm M, Guilbaud R, Watson M, Chelsky D, Davis C, Zetterberg H, Blennow K|
|Date/Time:||Thursday March 8, 2018 at 9:20am ET|
|Location:||Hilton Washington DC/Rockville|
Neurogranin and synaptotagmin-1 are synaptic proteins that are important for normal synapse function and plasticity. As a result of CNS synapse damage due to Alzheimer’s disease, concentrations of neurogranin and synaptotagmin-1 are significantly elevated in the cerebrospinal fluid (CSF) surrounding the brain compared to age-matched, cognitively normal individuals. In a Phase 1b/2a clinical study, treatment with Elayta for 28 days resulted in a statistically significant reduction in CSF concentrations of neurogranin and synaptotagmin-1 compared to placebo treatment.
The reductions of these synaptic damage proteins in the CSF are evidence of Elayta’s synaptoprotection mechanism of action in Alzheimer’s patients. Notably, these reductions are greater and more rapidly occurring than those reported for other candidate Alzheimer’s therapeutics.
Additional clinical trials are planned to assess the concentrations of these synapse damage biomarkers following longer term administration of Elayta.
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 beta amyloid (Aβ) oligomers 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 http://www.cogrx.com.
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.