Program
Preclinical
Phase 1
Phase 2
Phase 3
Status
Alzheimer's Disease
Early-to-mild AD
Phase 2 COG0203 • START
Actively recruiting​
Dementia with Lewy Bodies
Mild-to-moderate DLB
Phase 2 COG1201 • SHIMMER
Topline data ​2H-2024​
Dry Age-related Macular Degeneration
GA secondary to dry AMD
Phase 2 COG2201 • MAGNIFY
Actively recruiting​
Completed Studies
Mild-to-moderate AD
Phase 2 COG0201 • SHINE
Mild-to-moderate AD
Phase 2 COG0202 • SEQUEL (synaptic function)​
Mild-to-moderate AD
Phase 1 COG0105 • SPARC (synaptic density)​
Mild-to-moderate AD
Phase 1b COG0104 • SNAP (target engagement)​
CT1812: Modifying Disease to Change Disease Outcomes
Several neurodegenerative and neuro-ophthalmic diseases are caused by the age-related buildup of pathogenic proteins such as amyloid beta (Aβ) and alpha-synuclein as well as other stressors such as reactive oxygen species (ROS) and inflammatory signals. Left unchecked, these toxins can interfere with critical cellular functions, damage neurons and drive disease progression.
CT1812 is an oral therapy being developed to slow progression of Alzheimer’s disease, dementia with Lewy bodies (DLB) and dry age-related macular degeneration (dry AMD) by preserving the function of the sigma-2 receptor. This receptor regulates key processes that neurons and other cells employ to remove waste products and thus has the potential to protect cells from toxic buildup.
For more information on these four ongoing clinical trials, please visit our Clinical Trials webpage.
Sigma-2: The “Housekeeping” Receptor
Found in brain and retinal cells, the sigma-2 receptor complex is believed to function as the “housekeeper” of the brain’s neuronal network, regulating key pathways in age-related diseases like Alzheimer’s disease, dementia with Lewy bodies, and dry AMD.
Studies support that sigma-2 modulators can restore critical damage responses like protein trafficking and autophagy that are impaired in neurodegenerative diseases. In vitro studies of experimental sigma-2 receptor modulators demonstrated an ability to prevent the binding of Aβ oligomers to neurons and also to displace bound Aβ oligomers from neuronal receptors.