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Phase 2
Phase 3
Disruptions in Cellular Damage Response Drive Neurodegenerative Diseases
Alzheimer’s and Parkinson’s diseases and other neurodegenerative brain and eye disorders are caused by the age-related buildup of proteins such as beta amyloid (Aβ) and α-synuclein. Under normal conditions, cellular damage responses trigger the removal of these proteins before they are allowed to accumulate and aggregate into more toxic forms. However, in many neurodegenerative diseases, the damage response is disrupted, allowing the formation of toxic proteins, which in turn leads to damage and eventual loss of the neurons responsible for cognition in Alzheimer’s disease, cognitive and motor function in Parkinson’s disease, and sight in dry AMD.
Lead Candidate: CT1812
Cognition has identified several compounds that bind to a receptor that regulates the cellular damage response and have shown potential in the treatment of neurodegenerative diseases. The company’s lead candidate, CT1812, is a first-in-class, orally dosed and highly brain penetrant small molecule that is being assessed as a treatment for dementia with Lewy bodies, geographic atrophy secondary to dry AMD, as well as early and mild-to-moderate Alzheimer’s disease.
For more information on these four ongoing clinical trials, please visit our Clinical Trials webpage.