Pipeline

Program

Preclinical

Phase 1

Phase 2

Phase 3

Status

Alzheimer's Disease

Early-to-mild Alzheimer’s disease (AD)

Phase 2 COG0203 • START
Actively recruiting​

Dry Age-related Macular Degeneration

GA secondary to dry AMD
Phase 2 COG2201 • MAGNIFY **

Completed Studies

Mild-to-mod dementia with Lewy bodies (DLB)
Phase 2 COG1201 • SHIMMER
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)​
** NOTE: We made the strategic decision to voluntarily discontinue the MAGNIFY study to prioritize our resources on our ongoing programs in Alzheimer’s and dementia with Lewy bodies. The discontinuation was not the result of any safety concerns.​
Zervimesine: Modifying Disease to Change Disease Outcomes

Several neurodegenerative 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.

Zervimesine (also CT1812) is an oral therapy being developed to slow progression of Alzheimer’s disease and dementia with Lewy bodies (DLB) 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 our 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 and dementia with Lewy bodies. 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.
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