- Zervimesine (CT1812) shows promising neuroprotective effects in Alzheimer's disease.
- Phase 2 SEQUEL study demonstrates improvement in brain activity and neuron protection.
- Further research is needed to explore zervimesine's mechanism of action.
Cognition Therapeutics (CGTX, Financial) has published findings from its Phase 2 SEQUEL study, highlighting the potential benefits of zervimesine (CT1812) in protecting neurons and enhancing synaptic function in patients with mild-to-moderate Alzheimer's disease. The study demonstrated promising trends in normalizing brain electrical activity and improving neural communication, potentially slowing disease progression.
Analysis of the study data revealed that zervimesine affects critical proteins associated with vesicle formation, exocytosis, and endosomal trafficking, which are essential for neuronal health and synaptic plasticity. In vitro experiments further confirmed zervimesine's ability to protect neurons from oxidative stress-induced death and maintain cellular integrity by preventing the release of neurofilament light (NfL), a known marker of neuronal damage.
The SEQUEL study utilized quantitative electroencephalography (qEEG) to assess the drug's impact on brain activity, showing consistent improvements across prespecified EEG parameters. Notably, zervimesine reduced the prominence of theta waves, a frequency associated with Alzheimer's pathology, suggesting the drug's role in restoring healthier neural network function.
Although these findings align with previous results from the SHINE study, they primarily offer mechanistic insights rather than definitive clinical efficacy. Cognition Therapeutics plans to conduct further research to precisely understand how zervimesine prevents neuron death and to evaluate its long-term therapeutic effects in larger clinical trials.
