Mechanism of Action

Novel Mechanism of Action (MOA)

Dimebon (latrepirdine) has a unique mechanism of action, distinct from currently available treatments. In preclinical studies, dimebon has been shown to protect brain cells from damage and enhance brain cell survival, potentially by stabilizing and improving mitochondrial function.

Mitochondria and Cell Function

Mitochondria generate energy for cells and play important roles in mediating cell function and survival. Improved mitochondrial function has been correlated with increased synapse formation. Autopsy studies of brains from patients with Alzheimer's disease suggest that mitochondrial damage and synapse loss are early cellular events in Alzheimer's disease development and progression. Similarly, mitochondrial dysfunction has been linked to the progression of Huntington disease.

For more information on the role of mitochondria in Alzheimer's disease, please view the following video:

Dimebon MOA Studies

Preclinical data suggests that dimebon works through a different mechanism of action than other drugs that focus on targets implicated in cognition and memory loss, such as cholinesterase inhibition. In these experiments, dimebon was shown to be a weak cholinesterase inhibitor, and additional data from binding assays showed that dimebon did not have strong affinity to other standard targets.

Preclinical studies showed that dimebon preserved mitochondrial function after brain cells were challenged with different stressors including beta amyloid, a toxic substance often associated with Alzheimer’s disease and the loss of brain cells.