Thank You for Meeting Us
We enjoyed meeting you at the American Academy of Neurology meeting
Ongoing Clinical Programs
Indication
Preclinical
Phase 1
Phase 2
Phase 3
* Subject to discussion with FDA, this clinical development program will begin with a Phase 2 study supported by the Phase 1 AD studies
The sigma-2 (σ-2) receptor is expressed by multiple cell types, including neuronal synapses, and acts as a key regulator of cellular damage commonly associated with certain age-related degenerative diseases of the CNS and retina. The σ-2 complex is comprised of transmembrane protein 97 (TMEM97), a four-domain transmembrane protein that forms a complex with progesterone receptor membrane component 1 (PGRMC1).
The σ-2 complex is expressed in the CNS, the retina, as well as peripheral organs, including the pancreas, liver and kidney. Within the brain, the σ-2 complex is found in several areas, including the cerebellum, cortex, hippocampus and substantia nigra, and is enriched in neurons as compared to glial cells in the adult brain. In the retina, the σ-2 complex is expressed in several cell types including the RPE cells, photoreceptors and retinal ganglion cells.
We believe that targeting the σ-2 complex represents a mechanism that is functionally distinct from other current approaches in clinical development for the treatment of degenerative diseases.
Presentations and Publications
Cognition Therapeutics has several publications on the sigma-2 receptor, its role in neurological disorders such as Alzheimer’s disease and results of earlier studies. Select publications are listed below.
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Rishton GM, Look GC, Ni Z-J, et al. Discovery of Investigational Drug CT1812, an Antagonist of the Sigma-2 Receptor Complex for Alzheimer’s Disease. ACS Med Chem Lett. 2021 Aug 9;12(9):1389-1395.
Izzo NJ, Yuede CM, LaBarbera KM, et al. Preclinical and clinical biomarker studies of CT1812: A novel approach to Alzheimer’s disease modification. Alzheimer’s Dement. 2021 Aug; 17(8):1365-1382
Limegrover CS, LeVine H III, Izzo NJ, et al. Alzheimer’s Protection Effect of A673T Mutation May Be Driven by Lower Aβ Oligomer Binding Affinity. J Neurochem. 2020; 00: 1– 15. doi:10.1111/jnc.15212
