Cognition Therapeutics is focused on developing innovative therapies for neurodegenerative diseases, particularly Alzheimer's disease, dementia with Lewy bodies, and dry age-related macular degeneration (AMD). Their lead product candidate, CT1812, is a small-molecule drug designed to address cellular damage response mechanisms that are impaired in these conditions. By targeting the sigma-2 receptor, CT1812 aims to displace toxic protein oligomers that disrupt neuronal function, thereby potentially restoring normal cellular processes and protecting neurons from further damage. This mechanism of action is crucial for maintaining neuronal health and may slow the progression of these debilitating diseases.

In addition to its application in Alzheimer's disease, CT1812 shows promise in treating dementia with Lewy bodies and dry AMD. The drug is capable of crossing the blood-retinal barrier, which allows it to protect retinal pigment epithelial cells from damage, a critical function for maintaining vision. The ongoing clinical trials and research efforts underscore the potential of CT1812 to not only mitigate the effects of toxic protein accumulation but also to enhance the overall health of neurons in the brain and eye, offering hope for patients suffering from these neurodegenerative disorders.

United States

Cognition Therapeutics, Inc., a clinical-stage biopharmaceutical company, engages in the discovery and development of small molecule therapeutics targeting age-related degenerative diseases and disorders of the central nervous system and retina. Its lead product candidate is CT1812, a sigma-2 receptor antagonist, which is in phase 2 clinical trial for the treatment of mild-to-moderate Alzheimer’s disease, as well as has completed phase 1 clinical trial to treat early-stage Alzheimer’s disease; and in preclinical trial to treat dementia with Lewy bodies (DLB) and dry age-related macular degeneration (AMD). The company is also developing CT2168 for the treatment of synucleinopathies, which include DLB and Parkinson’s disease; and CT2074 to treat dry AMD. Cognition Therapeutics, Inc. was incorporated in 2007 and is headquartered in Purchase, New York.

Central Nervous System (CNS)

Eye Diseases

Nervous System Diseases

Cognition Therapeutics

Alzheimer's disease

Cognition’s approach is unique in that its candidate, CT1812, is &nbsp;designed to restore damaged cellular processes such as autophagy, &nbsp;cholesterol synthesis and protein trafficking, which are dysregulated in &nbsp;neurodegenerative disorders. CT1812 binds to TMEM97, a protein &nbsp;component of the σ-2 receptor, a key regulator of the cellular damage &nbsp;response. In Alzheimer’s disease, this results in the displacement of Aβ &nbsp;oligomers, which are then cleared into the CSF.
Preclinical studies have shown that by displacing Aβ oligomers and &nbsp;preventing further oligomer binding, the brain’s damage control &nbsp;mechanisms can be re-enabled. So long as the neurons remain viable, &nbsp;synaptic density and function can recover. This creates the opportunity &nbsp;to treat ongoing cognitive deficits in Alzheimer’s disease and prevent &nbsp;further deficits from occurring.
<a href="https://cogrx.com/pipeline-v1/neurodegenerative-diseases/">Source</a>

Zervimesine (CT1812) 

CT1812 is an experimental, orally delivered, small molecule designed to penetrate the blood-brain barrier and bind selectively to the sigma-2 (σ-2) receptor complex. The σ-2 receptor complex is involved in the regulation of key cellular processes such as membrane trafficking and autophagy that are damaged by toxic interaction with Aβ oligomers, oxidative stress and other stressors. This damage to sensitive synapses can progress to a loss of synaptic function, which manifests as cognitive impairment and Alzheimer’s disease progression.&nbsp;
 
Cognition’s approach is unique in that its candidate, CT1812, is &nbsp;designed to restore damaged cellular processes such as autophagy, &nbsp;cholesterol synthesis and protein trafficking, which are dysregulated in &nbsp;neurodegenerative disorders. CT1812 binds to TMEM97, a protein &nbsp;component of the σ-2 receptor, a key regulator of the cellular damage &nbsp;response. In Alzheimer’s disease, this results in the displacement of Aβ &nbsp;oligomers, which are then cleared into the CSF.
 
Preclinical studies have shown that by displacing Aβ oligomers and &nbsp;preventing further oligomer binding, the brain’s damage control &nbsp;mechanisms can be re-enabled. So long as the neurons remain viable, &nbsp;synaptic density and function can recover. This creates the opportunity &nbsp;to treat ongoing cognitive deficits in Alzheimer’s disease and prevent &nbsp;further deficits from occurring.
<a href="https://cogrx.com/pipeline-v1/neurodegenerative-diseases/">Source</a>

Cognition Therapeutics

Company Details