Company Overview of Cognition Therapeutics, Inc.
Cognition Therapeutics, Inc., a drug discovery company, develops small molecule therapeutics for Alzheimer's and other neurodegenerative diseases. Its products targets the toxic proteins that cause the cognitive decline associated with Alzheimer's disease and other degenerative diseases of the human brain. The company was incorporated in 2007 and is based in Pittsburgh, Pennsylvania.
2403 Sidney Street
Pittsburgh, PA 15203
Founded in 2007
Key Executives for Cognition Therapeutics, Inc.
Chief Executive Officer and President
Chief Medicinal Chemistry Advisor
Compensation as of Fiscal Year 2016.
Cognition Therapeutics, Inc. Key Developments
Cognition Therapeutics, Inc. Presents at 1st Annual Neuroscience BioPartnering & Investment Forum, Feb-23-2016 10:20 AM
Feb 23 16
Cognition Therapeutics, Inc. Presents at 1st Annual Neuroscience BioPartnering & Investment Forum, Feb-23-2016 10:20 AM. Venue: The New York Academy of Sciences, 7 World Trade Center, 250 Greenwich St, 40th Floor (D Elevator Bank), New York, NY 10007, United States.
Cognition Therapeutics, Inc. Presents at 8th Annual Biotech Showcase Investor Conference 2016, Jan-13-2016 11:15 AM
Dec 8 15
Cognition Therapeutics, Inc. Presents at 8th Annual Biotech Showcase Investor Conference 2016, Jan-13-2016 11:15 AM. Venue: Parc 55 San Francisco, 55 Cyril Magnin Street, San Francisco, CA 94102, United States.
Cognition Therapeutics Inc. Announces Publication of Research Identifying Sigma-2/PGRMC1 Receptor as Major New Drug Target for Alzheimer's Disease Therapy
Nov 12 14
Cognition Therapeutics Inc. announced the publication online of two articles entitled: Alzheimer's therapeutics targeting Amyloid beta 1-42 oligomers I: Abeta oligomers binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits and Alzheimers therapeutics targeting Amyloid beta 1-42 oligomers II: sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity, in PLOS ONE, the peer-reviewed open access science and medicine journal. Together these articles describe the coincident discovery of a major new drug target in the human brain implicated in Alzheimer's disease and a series of investigational drug candidates, which potentially can halt and reverse the insidious and devastating memory loss that Alzheimer's brings. Sigma-2/PGRMC1 receptor, the new Alzheimer's drug target, mediates the pathological effects of the water-soluble oligomeric version of amyloid beta 1-42 protein (Abeta), the agent widely thought to be a major causative factor of Alzheimer's disease. The first article in PLOS, entitled Alzheimer's therapeutics targeting Amyloid beta 1-42 oligomers I: Abeta oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits, describes company's Alzheimer's screening platform and proprietary CNS-biased compound library and its discovery of a set of candidate agents that are capable of blocking the toxic effects of both synthetic and human Abeta oligomers on processes important to neuronal cell communication and viability and ultimately memory formation and consolidation. The company's compounds prevent Abeta-induced neuronal degeneration in a mouse brain cell culture system and reverse Abeta-induced memory deficits in preclinical rodent models of memory and learning using both normal and APP-Swedish London transgenic mice. In the second article, entitled Alzheimers therapeutics targeting Amyloid beta 1-42 oligomers II: sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity, the company screened its compounds in industry-standard counterscreening assays to determine which receptors the compounds bound to. Sigma-2/PGRMC1 receptor protein was the only receptor that the compounds bound to with significant affinity, and further studies suggested it to be a major pharmacologically tractable target for Abeta toxicity in human brain. Sigma-2/PGRMC1 plays an important role in controlling whether or not certain proteins that are required for normal memory formation are located on the surface of brain cells. When Abeta builds up in the brain, as can be seen in older humans or Down's syndrome individuals, it forms oligomers that stick to the brain cell synapses and result in the reduction of proteins that are required for normal memory formation. The findings reported here make an important link between these two observations, and suggest that oligomer interactions with sigma-2/PGRMC1 may lead directly to this reduction.
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