Cognition Therapeutics Completes Enrollment in Phase 2 SHIMMER Study of CT1812 in Mild-to-Moderate Dementia with Lewy Bodies - Seite 2

About CT1812
CT1812 is an experimental orally delivered small molecule that penetrates the blood-brain barrier and binds selectively to the sigma-2 (σ-2) receptor complex, which is involved in the regulation of key cellular processes such as membrane trafficking and autophagy. These processes are disrupted by toxic interaction with oligomers of Aβ or α-synuclein, oxidative stress and other drivers of neurodegenerative disease. The ensuing damage to sensitive synapses can progress to a loss of synaptic function, which manifests as cognitive impairment, loss of motor or executive function and progression of disease.

CT1812 is currently being studied in several clinical trials, including the aforementioned SHIMMER study; two Phase 2 studies in Alzheimer’s disease including the START study (NCT05531656) in adults with MCI or early Alzheimer’s disease and the SHINE study (NCT03507790), which has concluded enrollment in adults with mild-to-moderate disease; and the MAGNIFY study (NCT05893537) in adults with geographic atrophy (GA) secondary to dry age-related macular degeneration.

The company expects to report topline results from the Phase 2 SHINE clinical trial in mid-2024. A virtual KOL event was conducted recently with experts who discussed, the currently approved immunotherapies for early Alzheimer’s disease, their commercial uptake, and the potential for other therapeutic modalities to improve upon their clinical effectiveness through combination or sequential therapy. The archive of this event may be viewed here: https://lifescievents.com/event/cognition/.

About Dementia with Lewy Bodies
An estimated 1.4 million Americans are living with DLB, a progressive disease that accounts for approximately 5-10% of all dementia cases. Approximately 50% of people with DLB have Aβ co-pathology as well as symptomology of Parkinson’s and Alzheimer’s diseases, making it challenging to diagnose. DLB is caused by a build-up of a protein, α-synuclein, which forms deposits, called Lewy bodies, in the brain. Oligomers of α-synuclein are highly toxic and bind to neurons where they impair critical cellular processes, causing synaptic dysfunction and loss. Patients with DLB often experience cognitive, physical, sleep and behavioral symptoms, including hallucinations, delusions and mood changes. There are currently no disease-modifying treatments approved for DLB patients.