Alzheimer’s disease is believed to be caused, in part, by the age-related buildup of proteins including amyloid beta (Aβ).
Under normal conditions, these proteins are removed from the brain before they accumulate and aggregate into more toxic forms, called oligomers. When this function is disrupted, the formation of toxic oligomers can lead to neurodegenerative disorders such as Alzheimer’s disease. These toxic oligomers bind to synapses and cause a cascade of damage resulting eventually in the loss of neurons and cognitive dysfunction.
Many development efforts for treating Alzheimer’s disease have focused on removing the buildup of Aβ plaques from the brain. Our scientific approach builds on these modern treatment advances. Our hypothesis, supported by preclinical and early clinical data, is that preventing toxic Aβ oligomers from binding to synapses – where they initiate damage – is a promising approach to slowing neuronal decline in Alzheimer’s disease. 

Cognition Therapeutics is currently developing zervimesine (CT1812), an investigational, brain-penetrant small-molecule oral therapy that has potential to protect synapses before irreversible neuronal decline, by displacing toxic Aβ oligomers from neuronal receptors.
Zervimesine has the potential to work in synergy with recently approved monoclonal antibody treatments. Due to its unique mechanism of action and favorable safety profile, zervimesine has the potential to complement treatments that remove plaques or impact other disease mechanisms by playing the vital role of synaptic protector.
Watch our mechanism of action video to learn more. »
SHINE COG0201 study:
- Complete with results: 153 adults with mild-to-moderate Alzheimer’s disease were randomized to receive one of two doses of zervimesine or placebo.
- Supported by appx $31 million in grant awards from the National Institute on Aging (NIA) of the National Institutes of Health (NIH).
- On July 29, 2024, a webcast was held to review findings from the SHINE study. Click here for the archive.
- Cognition conducted a second call on October 30, 2024 to review findings of a pre-specified analysis of SHINE subgroups defined by their baseline plasma p-tau217 concentrations. An archive of this call and supporting materials may be found here.
- For more information, please visit clinicatrials.gov and reference NCT03507790.
SEQUEL COG0202 study:
- Assessed disease-modification as a function of synapse function as measured by qualitative EEG.
- Topline results showed improvements in global measures of brain activity.
- For more information, please visit clinicatrials.gov and reference NCT04735536.
- Background information on qEEG and a summary of topline results maybe found here.
SNAP COG0104 study:
- Assessed target engagement vis-a-vis displacement of Aβ oligomers.
- For more information, please visit clinicaltrials.gov and reference NCT03522129.
SPARC COG0105 study:
- Assessed disease-modification as a measure of synapse density with PET imaging.
- For more information, please visit clinicaltrials.gov and reference NCT03493282.
Phase 1b/2a COG0102 study:
- Zervimesine was generally safe and tolerated in patients with mild-to-moderate Alzheimer’s disease.
- All adverse events were mild or moderate; there were no serious adverse events.
- Zervimesine achieved CSF concentrations greater than 80 percent estimated brain receptor occupancy, a level previously demonstrated in preclinical studies to be the minimum efficacious dose.
- Protein biomarkers associated with Alzheimer’s disease changed differentially in zervimesine-treated vs. placebo patients.
- For more information, please visit clinicaltrials.gov and reference NCT02907567.
START COG0203 study:
- Phase 2 study in early Alzheimer’s disease in collaboration with the Alzheimer’s Clinical Trials Consortium (ACTC).
- Target enrollment: 540
- Supported by a $81 million grant from the National Institute on Aging (NIA) of the National Institutes of Health (NIH).
- For more information, please visit start-study.org or clinicatrials.gov and reference NCT05531656.